@article {49827, title = {Dual Transcriptome Profiling of Leishmania-Infected Human Macrophages Reveals Distinct Reprogramming Signatures}, journal = {mBio}, volume = {7}, year = {2016}, month = {Jun-07-2016}, pages = {e00027-16}, doi = {10.1128/mBio.00027-16}, url = {http://mbio.asm.org/lookup/doi/10.1128/mBio.00027-16https://syndication.highwire.org/content/doi/10.1128/mBio.00027-16}, author = {Fernandes, Maria Cecilia and Dillon, Laura A. L. and Belew, Ashton Trey and Bravo, H{\'e}ctor Corrada and Mosser, David M. and El-Sayed, Najib M.} } @article {49840, title = {Identification guide to the heterobranch sea slugs (Mollusca: Gastropoda) from Bocas del Toro, Panama}, journal = {Marine Biodiversity Records}, volume = {96737453830254034557880541418411912544728739317415779780725696418782226404216145163412560451520488424050829677}, year = {2016}, month = {Jan-12-2016}, doi = {10.1186/s41200-016-0048-z}, url = {http://mbr.biomedcentral.com/articles/10.1186/s41200-016-0048-zhttp://link.springer.com/content/pdf/10.1186/s41200-016-0048-z}, author = {Goodheart, Jessica and Ellingson, Ryan A. and Vital, Xochitl G. and {\~a}o Filho, Hilton C. and McCarthy, Jennifer B. and Medrano, Sabrina M. and Bhave, Vishal J. and {\'\i}a-M{\'e}ndez, Kimberly and {\'e}nez, Lina M. and {\'o}pez, Gina and Hoover, Craig A. and Awbrey, Jaymes D. and De Jesus, Jessika M. and Gowacki, William and Krug, Patrick J. and {\'e}s, {\'A}ngel} } @article {49821, title = {Longitudinal analysis of the lung microbiota of cynomolgous macaques during long-term SHIV infection}, journal = {Microbiome}, volume = {4320384718719152130282021211818418719223326578105723}, year = {2016}, month = {Jan-12-2016}, doi = {10.1186/s40168-016-0183-0}, url = {http://microbiomejournal.biomedcentral.com/articles/10.1186/s40168-016-0183-0http://link.springer.com/content/pdf/10.1186/s40168-016-0183-0}, author = {Morris, Alison and Paulson, Joseph N. and Talukder, Hisham and Tipton, Laura and Kling, Heather and Cui, Lijia and Fitch, Adam and Pop, Mihai and Norris, Karen A. and Ghedin, Elodie} } @article {49817, title = {Therapeutic relevance of the protein phosphatase 2A in cancer}, journal = {Oncotarget.com}, year = {2016}, month = {Jul-09-2017}, doi = {10.18632/oncotarget.11399}, url = {https://www.oncotarget.com/article/11399}, author = {Cunningham, Chelsea E. and Li, Shuangshuang and Vizeacoumar, Frederick S. and Bhanumathy, Kalpana Kalyanasundaram and Lee, Joo Sang and Parameswaran, Sreejit and Furber, Levi and Abuhussein, Omar and Paul, James M. and McDonald, Megan and Templeton, Shaina D. and Shukla, Hersh and El Zawily, Amr M. and Boyd, Frederick and Alli, Nezeka and Mousseau, Darrell D. and Geyer, Ron and Bonham, Keith and Anderson, Deborah H. and Yan, Jiong and Yu-Lee, Li-Yuan and Weaver, Beth A. and Uppalapati, Maruti and Ruppin, Eytan and Sablina, Anna and Freywald, Andrew and Vizeacoumar, Franco J.} } @article {49579, title = {Fumarate induces redox-dependent senescence by modifying glutathione metabolism.}, volume = {6}, year = {2015}, month = {2015}, pages = {6001}, abstract = {

Mutations in the tricarboxylic acid (TCA) cycle enzyme fumarate hydratase (FH) are associated with a highly malignant form of renal cancer. We combined analytical chemistry and metabolic computational modelling to investigate the metabolic implications of FH loss in immortalized and primary mouse kidney cells. Here, we show that the accumulation of fumarate caused by the inactivation of FH leads to oxidative stress that is mediated by the formation of succinicGSH, a covalent adduct between fumarate and glutathione. Chronic succination of GSH, caused by the loss of FH, or by exogenous fumarate, leads to persistent oxidative stress and cellular senescence in vitro and in vivo. Importantly, the ablation of p21, a key mediator of senescence, in Fh1-deficient mice resulted in the transformation of benign renal cysts into a hyperplastic lesion, suggesting that fumarate-induced senescence needs to be bypassed for the initiation of renal cancers.

}, issn = {2041-1723}, doi = {10.1038/ncomms7001}, author = {Zheng, Liang and Cardaci, Simone and Jerby, Livnat and MacKenzie, Elaine D and Sciacovelli, Marco and Johnson, T Isaac and Gaude, Edoardo and King, Ayala and Leach, Joshua D G and Edrada-Ebel, RuAngelie and Hedley, Ann and Morrice, Nicholas A and Kalna, Gabriela and Blyth, Karen and Ruppin, Eytan and Frezza, Christian and Gottlieb, Eyal} } @article {49538, title = {The generation of macrophages with anti-inflammatory activity in the absence of STAT6 signaling.}, volume = {98}, year = {2015}, month = {2015 Sep}, pages = {395-407}, abstract = {

Macrophages readily change their phenotype in response to exogenous stimuli. In this work, macrophages were stimulated under a variety of experimental conditions, and phenotypic alterations were correlated with changes in gene expression. We identified 3 transcriptionally related populations of macrophages with immunoregulatory activity. They were generated by stimulating cells with TLR ligands in the presence of 3 different "reprogramming" signals: high-density ICs, PGE2, or Ado. All 3 of these cell populations produced high levels of transcripts for IL-10 and growth and angiogenic factors. They also secreted reduced levels of inflammatory cytokines IL-1β, IL-6, and IL-12. All 3 macrophage phenotypes could partially rescue mice from lethal endotoxemia, and therefore, we consider each to have anti-inflammatory activity. This ability to regulate innate-immune responses occurred equally well in macrophages from STAT6-deficient mice. The lack of STAT6 did not affect the ability of macrophages to change cytokine production reciprocally or to rescue mice from lethal endotoxemia. Furthermore, treatment of macrophages with IL-4 failed to induce similar phenotypic or transcriptional alterations. This work demonstrates that there are multiple ways to generate macrophages with immunoregulatory activity. These anti-inflammatory macrophages are transcriptionally and functionally related to each other and are quite distinct from macrophages treated with IL-4.

}, issn = {1938-3673}, doi = {10.1189/jlb.2A1114-560R}, author = {Fleming, Bryan D and Chandrasekaran, Prabha and Dillon, Laura A L and Dalby, Elizabeth and Suresh, Rahul and Sarkar, Arup and El-Sayed, Najib M and Mosser, David M} } @article {49734, title = {Genomic variation. Impact of regulatory variation from RNA to protein.}, journal = {Science}, volume = {347}, year = {2015}, month = {2015 Feb 6}, pages = {664-7}, abstract = {

The phenotypic consequences of expression quantitative trait loci (eQTLs) are presumably due to their effects on protein expression levels. Yet the impact of genetic variation, including eQTLs, on protein levels remains poorly understood. To address this, we mapped genetic variants that are associated with eQTLs, ribosome occupancy (rQTLs), or protein abundance (pQTLs). We found that most QTLs are associated with transcript expression levels, with consequent effects on ribosome and protein levels. However, eQTLs tend to have significantly reduced effect sizes on protein levels, which suggests that their potential impact on downstream phenotypes is often attenuated or buffered. Additionally, we identified a class of cis QTLs that affect protein abundance with little or no effect on messenger RNA or ribosome levels, which suggests that they may arise from differences in posttranslational regulation.

}, keywords = {3{\textquoteright} Flanking Region, 5{\textquoteright} Flanking Region, Cell Line, Exons, Gene Expression Regulation, Genetic Variation, HUMANS, PHENOTYPE, Protein Biosynthesis, Quantitative Trait Loci, Ribosomes, RNA, Messenger, Transcription, Genetic}, issn = {1095-9203}, doi = {10.1126/science.1260793}, author = {Battle, Alexis and Khan, Zia and Wang, Sidney H and Mitrano, Amy and Ford, Michael J and Pritchard, Jonathan K and Gilad, Yoav} } @article {49659, title = {Glutamine synthetase activity fuels nucleotide biosynthesis and supports growth of glutamine-restricted glioblastoma}, journal = {Nature Cell Biology}, volume = {17}, year = {2015}, month = {Nov-11-2016}, pages = {1556 - 1568}, issn = {1465-7392}, doi = {10.1038/ncb3272}, url = {http://www.nature.com/doifinder/10.1038/ncb3272}, author = {Tardito, Saverio and Oudin, {\"\i}s and Ahmed, Shafiq U. and Fack, Fred and Keunen, Olivier and Zheng, Liang and Miletic, Hrvoje and Sakariassen, {\O}ystein and Weinstock, Adam and Wagner, Allon and Lindsay, Susan L. and Hock, Andreas K. and Barnett, Susan C. and Ruppin, Eytan and {\o}rkve, Svein Harald and Lund-Johansen, Morten and Chalmers, Anthony J. and Bjerkvig, Rolf and Niclou, Simone P. and Gottlieb, Eyal} } @article {49540, title = {Impact of regulatory variation from RNA to protein}, volume = {347}, year = {2015}, month = {Jun-02-2015}, pages = {664 - 667}, issn = {0036-8075}, doi = {10.1126/science.1260793}, url = {http://www.sciencemag.org/cgi/doi/10.1126/science.1260793}, author = {Battle, A. and Khan, Z. and Wang, S. H. and Mitrano, A. and Ford, M. J. and Pritchard, J. K. and Gilad, Y.} } @article {49575, title = {Improved evidence-based genome-scale metabolic models for maize leaf, embryo, and endosperm.}, volume = {6}, year = {2015}, month = {2015}, pages = {142}, abstract = {

There is a growing demand for genome-scale metabolic reconstructions for plants, fueled by the need to understand the metabolic basis of crop yield and by progress in genome and transcriptome sequencing. Methods are also required to enable the interpretation of plant transcriptome data to study how cellular metabolic activity varies under different growth conditions or even within different organs, tissues, and developmental stages. Such methods depend extensively on the accuracy with which genes have been mapped to the biochemical reactions in the plant metabolic pathways. Errors in these mappings lead to metabolic reconstructions with an inflated number of reactions and possible generation of unreliable metabolic phenotype predictions. Here we introduce a new evidence-based genome-scale metabolic reconstruction of maize, with significant improvements in the quality of the gene-reaction associations included within our model. We also present a new approach for applying our model to predict active metabolic genes based on transcriptome data. This method includes a minimal set of reactions associated with low expression genes to enable activity of a maximum number of reactions associated with high expression genes. We apply this method to construct an organ-specific model for the maize leaf, and tissue specific models for maize embryo and endosperm cells. We validate our models using fluxomics data for the endosperm and embryo, demonstrating an improved capacity of our models to fit the available fluxomics data. All models are publicly available via the DOE Systems Biology Knowledgebase and PlantSEED, and our new method is generally applicable for analysis transcript profiles from any plant, paving the way for further in silico studies with a wide variety of plant genomes.

}, issn = {1664-462X}, doi = {10.3389/fpls.2015.00142}, author = {Seaver, Samuel M D and Bradbury, Louis M T and Frelin, Oc{\'e}ane and Zarecki, Raphy and Ruppin, Eytan and Hanson, Andrew D and Henry, Christopher S} } @article {49512, title = {Independent Emergence of Artemisinin Resistance Mutations Among Plasmodium falciparum in Southeast Asia}, journal = {Journal of Infectious Diseases}, volume = {211}, year = {2015}, month = {03/2015}, pages = {670 - 679}, issn = {1537-6613}, doi = {10.1093/infdis/jiu491}, author = {Takala-Harrison, S. and Jacob, C. G. and Arze, C. and Michael P. Cummings and Silva, J. C. and Dondorp, A. M. and Fukuda, M. M. and Hien, T. T. and Mayxay, M. and Noedl, H. and Nosten, F. and Kyaw, M. P. and Nhien, N. T. T. and Imwong, M. and Bethell, D. and Se, Y. and Lon, C. and Tyner, S. D. and Saunders, D. L. and Ariey, F. and Mercereau-Puijalon, O. and Menard, D. and Newton, P. N. and Khanthavong, M. and Hongvanthong, B. and Starzengruber, P. and Fuehrer, H.-P. and Swoboda, P. and Khan, W. A. and Phyo, A. P. and Nyunt, M. M. and Nyunt, M. H. and Brown, T. S. and Adams, M. and Pepin, C. S. and Bailey, J. and Tan, J. C. and Ferdig, M. T. and Clark, T. G. and Miotto, O. and MacInnis, B. and Kwiatkowski, D. P. and White, N. J. and Ringwald, P. and Plowe, CV} } @article {49612, title = {Microbiota that affect risk for shigellosis in children in low-income countries}, journal = {Emerg Infect DisEmerg Infect Dis}, volume = {21}, number = {2}, year = {2015}, note = {Lindsay, Brianna
Oundo, Joe
Hossain, M Anowar
Antonio, Martin
Tamboura, Boubou
Walker, Alan W
Paulson, Joseph N
Parkhill, Julian
Omore, Richard
Faruque, Abu S G
Das, Suman Kumar
Ikumapayi, Usman N
Adeyemi, Mitchell
Sanogo, Doh
Saha, Debasish
Sow, Samba
Farag, Tamer H
Nasrin, Dilruba
Li, Shan
Panchalingam, Sandra
Levine, Myron M
Kotloff, Karen
Magder, Laurence S
Hungerford, Laura
Sommerfelt, Halvor
Pop, Mihai
Nataro, James P
Stine, O Colin
U19 090873/PHS HHS/United States
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov{\textquoteright}t
Research Support, U.S. Gov{\textquoteright}t, Non-P.H.S.
United States
Emerg Infect Dis. 2015 Feb;21(2):242-50. doi: 10.3201/eid2101.140795.}, month = {Feb}, pages = {242-50}, edition = {2015/01/28}, abstract = {Pathogens in the gastrointestinal tract exist within a vast population of microbes. We examined associations between pathogens and composition of gut microbiota as they relate to Shigella spp./enteroinvasive Escherichia coli infection. We analyzed 3,035 stool specimens (1,735 nondiarrheal and 1,300 moderate-to-severe diarrheal) from the Global Enteric Multicenter Study for 9 enteropathogens. Diarrheal specimens had a higher number of enteropathogens (diarrheal mean 1.4, nondiarrheal mean 0.95; p<0.0001). Rotavirus showed a negative association with Shigella spp. in cases of diarrhea (odds ratio 0.31, 95\% CI 0.17-0.55) and had a large combined effect on moderate-to-severe diarrhea (odds ratio 29, 95\% CI 3.8-220). In 4 Lactobacillus taxa identified by 16S rRNA gene sequencing, the association between pathogen and disease was decreased, which is consistent with the possibility that Lactobacillus spp. are protective against Shigella spp.-induced diarrhea. Bacterial diversity of gut microbiota was associated with diarrhea status, not high levels of the Shigella spp. ipaH gene.}, isbn = {1080-6059 (Electronic)
1080-6040 (Linking)}, author = {Lindsay, B. and Oundo, J. and Hossain, M. A. and Antonio, M. and Tamboura, B. and Walker, A. W. and Paulson, J. N. and Parkhill, J. and Omore, R. and Faruque, A. S. and Das, S. K. and Ikumapayi, U. N. and Adeyemi, M. and Sanogo, D. and Saha, D. and Sow, S. and Farag, T. H. and Nasrin, D. and Li, S. and Panchalingam, S. and Levine, M. M. and Kotloff, K. and Magder, L. S. and Hungerford, L. and Sommerfelt, H. and Pop, M. and Nataro, J. P. and Stine, O. C.} } @article {49513, title = {Plasmodium falciparum field isolates from areas of repeated emergence of drug resistant malaria show no evidence of hypermutator phenotype}, journal = {Infection, Genetics and Evolution}, volume = {30}, year = {2015}, month = {03/2015}, pages = {318 - 322}, issn = {15671348}, doi = {10.1016/j.meegid.2014.12.010}, author = {Brown, Tyler S. and Jacob, Christopher G and Silva, Joana C and Takala-Harrison, Shannon and Djimd{\'e}, Abdoulaye and Dondorp, Arjen M and Fukuda, Mark and Noedl, Harald and Nyunt, Myaing Myaing and Kyaw, Myat Phone and Mayxay, Mayfong and Hien, Tran Tinh and Plowe, Christopher V and Michael P. Cummings} } @article {49577, title = {Proteomics-based metabolic modeling reveals that fatty acid oxidation (FAO) controls endothelial cell (EC) permeability.}, volume = {14}, year = {2015}, month = {2015 Mar}, pages = {621-34}, abstract = {

Endothelial cells (ECs) play a key role to maintain the functionality of blood vessels. Altered EC permeability causes severe impairment in vessel stability and is a hallmark of pathologies such as cancer and thrombosis. Integrating label-free quantitative proteomics data into genome-wide metabolic modeling, we built up a model that predicts the metabolic fluxes in ECs when cultured on a tridimensional matrix and organize into a vascular-like network. We discovered how fatty acid oxidation increases when ECs are assembled into a fully formed network that can be disrupted by inhibiting CPT1A, the fatty acid oxidation rate-limiting enzyme. Acute CPT1A inhibition reduces cellular ATP levels and oxygen consumption, which are restored by replenishing the tricarboxylic acid cycle. Remarkably, global phosphoproteomic changes measured upon acute CPT1A inhibition pinpointed altered calcium signaling. Indeed, CPT1A inhibition increases intracellular calcium oscillations. Finally, inhibiting CPT1A induces hyperpermeability in vitro and leakage of blood vessel in vivo, which were restored blocking calcium influx or replenishing the tricarboxylic acid cycle. Fatty acid oxidation emerges as central regulator of endothelial functions and blood vessel stability and druggable pathway to control pathological vascular permeability.

}, issn = {1535-9484}, doi = {10.1074/mcp.M114.045575}, author = {Patella, Francesca and Schug, Zachary T and Persi, Erez and Neilson, Lisa J and Erami, Zahra and Avanzato, Daniele and Maione, Federica and Hernandez-Fernaud, Juan R and Mackay, Gillian and Zheng, Liang and Reid, Steven and Frezza, Christian and Giraudo, Enrico and Fiorio Pla, Alessandra and Anderson, Kurt and Ruppin, Eytan and Gottlieb, Eyal and Zanivan, Sara} } @article {49539, title = {Transcriptomic profiling of gene expression and RNA processing during Leishmania major differentiation.}, volume = {43}, year = {2015}, month = {2015 Aug 18}, pages = {6799-813}, abstract = {

Protozoan parasites of the genus Leishmania are the etiological agents of leishmaniasis, a group of diseases with a worldwide incidence of 0.9-1.6 million cases per year. We used RNA-seq to conduct a high-resolution transcriptomic analysis of the global changes in gene expression and RNA processing events that occur as L. major transforms from non-infective procyclic promastigotes to infective metacyclic promastigotes. Careful statistical analysis across multiple biological replicates and the removal of batch effects provided a high quality framework for comprehensively analyzing differential gene expression and transcriptome remodeling in this pathogen as it acquires its infectivity. We also identified precise 5{\textquoteright} and 3{\textquoteright} UTR boundaries for a majority of Leishmania genes and detected widespread alternative trans-splicing and polyadenylation. An investigation of possible correlations between stage-specific preferential trans-splicing or polyadenylation sites and differentially expressed genes revealed a lack of systematic association, establishing that differences in expression levels cannot be attributed to stage-regulated alternative RNA processing. Our findings build on and improve existing expression datasets and provide a substantially more detailed view of L. major biology that will inform the field and potentially provide a stronger basis for drug discovery and vaccine development efforts.

}, issn = {1362-4962}, doi = {10.1093/nar/gkv656}, author = {Dillon, Laura A L and Okrah, Kwame and Hughitt, V Keith and Suresh, Rahul and Li, Yuan and Fernandes, Maria Cecilia and Belew, A Trey and Corrada Bravo, Hector and Mosser, David M and El-Sayed, Najib M} } @article {49863, title = {Complete genome sequence of the quality control strain Staphylococcus aureus subsp. aureus ATCC 25923}, journal = {Genome announcements}, volume = {2}, year = {2014}, pages = {e01110{\textendash}14}, author = {Treangen, Todd J and Maybank, Rosslyn A and Enke, Sana and Friss, Mary Beth and Diviak, Lynn F and Karaolis, David KR and Koren, Sergey and Ondov, Brian and Phillippy, Adam M and Bergman, Nicholas H} } @article {49725, title = {A computational study of the Warburg effect identifies metabolic targets inhibiting cancer migration.}, journal = {Mol Syst Biol}, volume = {10}, year = {2014}, month = {2014}, pages = {744}, abstract = {

Over the last decade, the field of cancer metabolism has mainly focused on studying the role of tumorigenic metabolic rewiring in supporting cancer proliferation. Here, we perform the first genome-scale computational study of the metabolic underpinnings of cancer migration. We build genome-scale metabolic models of the NCI-60 cell lines that capture the Warburg effect (aerobic glycolysis) typically occurring in cancer cells. The extent of the Warburg effect in each of these cell line models is quantified by the ratio of glycolytic to oxidative ATP flux (AFR), which is found to be highly positively associated with cancer cell migration. We hence predicted that targeting genes that mitigate the Warburg effect by reducing the AFR may specifically inhibit cancer migration. By testing the anti-migratory effects of silencing such 17 top predicted genes in four breast and lung cancer cell lines, we find that up to 13 of these novel predictions significantly attenuate cell migration either in all or one cell line only, while having almost no effect on cell proliferation. Furthermore, in accordance with the predictions, a significant reduction is observed in the ratio between experimentally measured ECAR and OCR levels following these perturbations. Inhibiting anti-migratory targets is a promising future avenue in treating cancer since it may decrease cytotoxic-related side effects that plague current anti-proliferative treatments. Furthermore, it may reduce cytotoxic-related clonal selection of more aggressive cancer cells and the likelihood of emerging resistance.

}, issn = {1744-4292}, doi = {10.15252/msb.20145746}, author = {Yizhak, Keren and Le D{\'e}v{\'e}dec, Sylvia E and Rogkoti, Vasiliki Maria and Baenke, Franziska and de Boer, Vincent C and Frezza, Christian and Schulze, Almut and van de Water, Bob and Ruppin, Eytan} } @article {49581, title = {Integrating Transcriptomics with Metabolic Modeling Predicts Biomarkers and Drug Targets for Alzheimer{\textquoteright}s Disease}, volume = {9}, year = {2014}, month = {Mar-08-2015}, pages = {e105383}, doi = {10.1371/journal.pone.0105383}, url = {http://www.cs.tau.ac.il/~ruppin/ad_plos1.pdf}, author = {Stempler, Shiri and Yizhak, Keren and Ruppin, Eytan}, editor = {Fong, Stephen S.} } @article {49604, title = {Large hypomethylated blocks as a universal defining epigenetic alteration in human solid tumors.}, volume = {6}, year = {2014}, month = {2014}, pages = {61}, abstract = {

BACKGROUND: One of the most provocative recent observations in cancer epigenetics is the discovery of large hypomethylated blocks, including single copy genes, in colorectal cancer, that correspond in location to heterochromatic LOCKs (large organized chromatin lysine-modifications) and LADs (lamin-associated domains).

METHODS: Here we performed a comprehensive genome-scale analysis of 10 breast, 28 colon, nine lung, 38 thyroid, 18 pancreas cancers, and five pancreas neuroendocrine tumors as well as matched normal tissue from most of these cases, as well as 51 premalignant lesions. We used a new statistical approach that allows the identification of large hypomethylated blocks on the Illumina HumanMethylation450 BeadChip platform.

RESULTS: We find that hypomethylated blocks are a universal feature of common solid human cancer, and that they occur at the earliest stage of premalignant tumors and progress through clinical stages of thyroid and colon cancer development. We also find that the disrupted CpG islands widely reported previously, including hypermethylated island bodies and hypomethylated shores, are enriched in hypomethylated blocks, with flattening of the methylation signal within and flanking the islands. Finally, we found that genes showing higher between individual gene expression variability are enriched within these hypomethylated blocks.

CONCLUSION: Thus hypomethylated blocks appear to be a universal defining epigenetic alteration in human cancer, at least for common solid tumors.

}, issn = {1756-994X}, doi = {10.1186/s13073-014-0061-y}, author = {Timp, Winston and Bravo, H{\'e}ctor Corrada and McDonald, Oliver G and Goggins, Michael and Umbricht, Chris and Zeiger, Martha and Feinberg, Andrew P and Irizarry, Rafael A} } @article {49588, title = {Maximal Sum of Metabolic Exchange Fluxes Outperforms Biomass Yield as a Predictor of Growth Rate of Microorganisms}, volume = {9}, year = {2014}, month = {Mar-05-2016}, pages = {e98372}, doi = {10.1371/journal.pone.0098372}, url = {http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0098372}, author = {Zarecki, Raphy and Oberhardt, Matthew A. and Yizhak, Keren and Wagner, Allon and Shtifman Segal, Ella and Freilich, Shiri and Henry, Christopher S. and Gophna, Uri and Ruppin, Eytan}, editor = {Fong, Stephen S.} } @article {49605, title = {Minfi: a flexible and comprehensive Bioconductor package for the analysis of Infinium DNA methylation microarrays.}, volume = {30}, year = {2014}, month = {2014 May 15}, pages = {1363-9}, abstract = {

MOTIVATION: The recently released Infinium HumanMethylation450 array (the {\textquoteright}450k{\textquoteright} array) provides a high-throughput assay to quantify DNA methylation (DNAm) at \~{}450 000 loci across a range of genomic features. Although less comprehensive than high-throughput sequencing-based techniques, this product is more cost-effective and promises to be the most widely used DNAm high-throughput measurement technology over the next several years.

RESULTS: Here we describe a suite of computational tools that incorporate state-of-the-art statistical techniques for the analysis of DNAm data. The software is structured to easily adapt to future versions of the technology. We include methods for preprocessing, quality assessment and detection of differentially methylated regions from the kilobase to the megabase scale. We show how our software provides a powerful and flexible development platform for future methods. We also illustrate how our methods empower the technology to make discoveries previously thought to be possible only with sequencing-based methods.

AVAILABILITY AND IMPLEMENTATION: http://bioconductor.org/packages/release/bioc/html/minfi.html.

CONTACT: khansen@jhsph.edu; rafa@jimmy.harvard.edu

SUPPLEMENTARY INFORMATION: Supplementary data are available at Bioinformatics online.

}, keywords = {Aged, algorithms, Colonic Neoplasms, DNA Methylation, Genome, High-Throughput Nucleotide Sequencing, HUMANS, Oligonucleotide Array Sequence Analysis, Polymorphism, Single Nucleotide, software}, issn = {1367-4811}, doi = {10.1093/bioinformatics/btu049}, author = {Aryee, Martin J and Jaffe, Andrew E and Corrada-Bravo, Hector and Ladd-Acosta, Christine and Feinberg, Andrew P and Hansen, Kasper D and Irizarry, Rafael A} } @article {49724, title = {Phenotype-based cell-specific metabolic modeling reveals metabolic liabilities of cancer.}, journal = {Elife}, volume = {3}, year = {2014}, month = {2014}, abstract = {

Utilizing molecular data to derive functional physiological models tailored for specific cancer cells can facilitate the use of individually tailored therapies. To this end we present an approach termed PRIME for generating cell-specific genome-scale metabolic models (GSMMs) based on molecular and phenotypic data. We build >280 models of normal and cancer cell-lines that successfully predict metabolic phenotypes in an individual manner. We utilize this set of cell-specific models to predict drug targets that selectively inhibit cancerous but not normal cell proliferation. The top predicted target, MLYCD, is experimentally validated and the metabolic effects of MLYCD depletion investigated. Furthermore, we tested cell-specific predicted responses to the inhibition of metabolic enzymes, and successfully inferred the prognosis of cancer patients based on their PRIME-derived individual GSMMs. These results lay a computational basis and a counterpart experimental proof of concept for future personalized metabolic modeling applications, enhancing the search for novel selective anticancer therapies.

}, keywords = {algorithms, Antineoplastic Agents, Biomarkers, Tumor, Carboxy-Lyases, Cell Line, Tumor, Cell Proliferation, Citric Acid Cycle, Fatty Acids, Gene Knockdown Techniques, Genome, Human, HUMANS, Lymphocytes, Models, Biological, Neoplasms, Oxidation-Reduction, PHENOTYPE, Precision Medicine}, issn = {2050-084X}, doi = {10.7554/eLife.03641}, author = {Yizhak, Keren and Gaude, Edoardo and Le D{\'e}v{\'e}dec, Sylvia and Waldman, Yedael Y and Stein, Gideon Y and van de Water, Bob and Frezza, Christian and Ruppin, Eytan} } @article {49736, title = {Stoichiometry of site-specific lysine acetylation in an entire proteome.}, journal = {J Biol Chem}, volume = {289}, year = {2014}, month = {2014 Aug 1}, pages = {21326-38}, abstract = {

Acetylation of lysine ϵ-amino groups influences many cellular processes and has been mapped to thousands of sites across many organisms. Stoichiometric information of acetylation is essential to accurately interpret biological significance. Here, we developed and employed a novel method for directly quantifying stoichiometry of site-specific acetylation in the entire proteome of Escherichia coli. By coupling isotopic labeling and a novel pairing algorithm, our approach performs an in silico enrichment of acetyl peptides, circumventing the need for immunoenrichment. We investigated the function of the sole NAD(+)-dependent protein deacetylase, CobB, on both site-specific and global acetylation. We quantified 2206 peptides from 899 proteins and observed a wide distribution of acetyl stoichiometry, ranging from less than 1\% up to 98\%. Bioinformatic analysis revealed that metabolic enzymes, which either utilize or generate acetyl-CoA, and proteins involved in transcriptional and translational processes displayed the highest degree of acetylation. Loss of CobB led to increased global acetylation at low stoichiometry sites and induced site-specific changes at high stoichiometry sites, and biochemical analysis revealed altered acetyl-CoA metabolism. Thus, this study demonstrates that sirtuin deacetylase deficiency leads to both site-specific and global changes in protein acetylation stoichiometry, affecting central metabolism.

}, keywords = {Acetylation, Amino Acid Sequence, Bacterial Proteins, Chromatography, High Pressure Liquid, Computational Biology, Escherichia coli, Lysine, Molecular Sequence Data, Proteome, Tandem Mass Spectrometry}, issn = {1083-351X}, doi = {10.1074/jbc.M114.581843}, author = {Baeza, Josue and Dowell, James A and Smallegan, Michael J and Fan, Jing and Amador-Noguez, Daniel and Khan, Zia and Denu, John M} } @article {49828, title = {Contribution of nucleosome binding preferences and co-occurring DNA sequences to transcription factor binding}, journal = {BMC Genomics}, volume = {14}, year = {2013}, month = {Jan-01-2013}, pages = {428}, issn = {1471-2164}, doi = {10.1186/1471-2164-14-428}, url = {http://bmcgenomics.biomedcentral.com/articles/10.1186/1471-2164-14-428}, author = {He, Ximiao and Chatterjee, Raghunath and John, Sam and Bravo, Hector and Sathyanarayana, B K and Biddie, Simon C and FitzGerald, Peter C and Stamatoyannopoulos, John A and Hager, Gordon L and Vinson, Charles} } @article {38284, title = {Genetic loci associated with delayed clearance of Plasmodium falciparum following artemisinin treatment in Southeast Asia}, journal = {Proceedings of the National Academy of Sciences of the United States of AmericaProceedings of the National Academy of Sciences of the United States of America}, volume = {110}, year = {2013}, type = {10.1073/pnas.1211205110}, abstract = {The recent emergence of artemisinin-resistant Plasmodium falciparum malaria in western Cambodia could threaten prospects for malaria elimination. Identification of the genetic basis of resistance would provide tools for molecular surveillance, aiding efforts to contain resistance. Clinical trials of artesunate efficacy were conducted in Bangladesh, in northwestern Thailand near the Myanmar border, and at two sites in western Cambodia. Parasites collected from trial participants were genotyped at 8,079 single nucleotide polymorphisms (SNPs) using a P. falciparum-specific SNP array. Parasite genotypes were examined for signatures of recent positive selection and association with parasite clearance phenotypes to identify regions of the genome associated with artemisinin resistance. Four SNPs on chromosomes 10 (one), 13 (two), and 14 (one) were significantly associated with delayed parasite clearance. The two SNPs on chromosome 13 are in a region of the genome that appears to be under strong recent positive selection in Cambodia. The SNPs on chromosomes 10 and 13 lie in or near genes involved in postreplication repair, a DNA damage-tolerance pathway. Replication and validation studies are needed to refine the location of loci responsible for artemisinin resistance and to understand the mechanism behind it; however, two SNPs on chromosomes 10 and 13 may be useful markers of delayed parasite clearance in surveillance for artemisinin resistance in Southeast Asia.}, author = {Takala-Harrison, Shannon and Clark, Taane G. and Jacob, Christopher G. and Michael P. Cummings and Miotto, Olivo and Dondorp, Arjen M. and Fukuda, Mark M. and Nosten, Francois and Noedl, Harald and Imwong, Mallika and Bethell, Delia and Se, Youry and Lon, Chanthap and Tyner, Stuart D. and Saunders, David L. and Socheat, Duong and Ariey, Frederic and Phyo, Aung Pyae and Starzengruber, Peter and Fuehrer, Hans-Peter and Swoboda, Paul and Stepniewska, Kasia and Flegg, Jennifer and Arze, Cesar and Cerqueira, Gustavo C. and Silva, Joana C. and Ricklefs, Stacy M. and Porcella, Stephen F. and Stephens, Robert M. and Adams, Matthew and Kenefic, Leo J. and Campino, Susana and Auburn, Sarah and Macinnis, Bronwyn and Kwiatkowski, Dominic P. and Su, Xin-Zhuan and White, Nicholas J. and Ringwald, Pascal and Plowe, Christopher V.} } @article {49858, title = {Genome sequence of the attenuated Carbosap vaccine strain of Bacillus anthracis}, journal = {Genome announcements}, volume = {1}, year = {2013}, pages = {e00067{\textendash}12}, author = {Harrington, Robin and Ondov, Brian D and Radune, Diana and Friss, Mary Beth and Klubnik, Joy and Diviak, Lynn and Hnath, Jonathan and Cendrowski, Stephen R and Blank, Thomas E and Karaolis, David and Todd Treangen} } @article {49535, title = {Genomic analysis of sequence-dependent DNA curvature in Leishmania.}, volume = {8}, year = {2013}, month = {2013}, pages = {e63068}, abstract = {

Leishmania major is a flagellated protozoan parasite of medical importance. Like other members of the Trypanosomatidae family, it possesses unique mechanisms of gene expression such as constitutive polycistronic transcription of directional gene clusters, gene amplification, mRNA trans-splicing, and extensive editing of mitochondrial transcripts. The molecular signals underlying most of these processes remain under investigation. In order to investigate the role of DNA secondary structure signals in gene expression, we carried out a genome-wide in silico analysis of the intrinsic DNA curvature. The L. major genome revealed a lower frequency of high intrinsic curvature regions as well as inter- and intra- chromosomal distribution heterogeneity, when compared to prokaryotic and eukaryotic organisms. Using a novel method aimed at detecting region-integrated intrinsic curvature (RIIC), high DNA curvature was found to be associated with regions implicated in transcription initiation. Those include divergent strand-switch regions between directional gene clusters and regions linked to markers of active transcription initiation such as acetylated H3 histone, TRF4 and SNAP50. These findings suggest a role for DNA curvature in transcription initiation in Leishmania supporting the relevance of DNA secondary structures signals.

}, keywords = {Chromosome mapping, Comparative Genomic Hybridization, Computational Biology, DNA, Protozoan, Genome, Protozoan, Genomics, HUMANS, Leishmania, Nucleic Acid Conformation}, issn = {1932-6203}, doi = {10.1371/journal.pone.0063068}, author = {Smircich, Pablo and Forteza, Diego and El-Sayed, Najib M and Garat, Beatriz} } @article {49738, title = {Primate transcript and protein expression levels evolve under compensatory selection pressures.}, journal = {Science}, volume = {342}, year = {2013}, month = {2013 Nov 29}, pages = {1100-4}, abstract = {

Changes in gene regulation have likely played an important role in the evolution of primates. Differences in messenger RNA (mRNA) expression levels across primates have often been documented; however, it is not yet known to what extent measurements of divergence in mRNA levels reflect divergence in protein expression levels, which are probably more important in determining phenotypic differences. We used high-resolution, quantitative mass spectrometry to collect protein expression measurements from human, chimpanzee, and rhesus macaque lymphoblastoid cell lines and compared them to transcript expression data from the same samples. We found dozens of genes with significant expression differences between species at the mRNA level yet little or no difference in protein expression. Overall, our data suggest that protein expression levels evolve under stronger evolutionary constraint than mRNA levels.

}, keywords = {Animals, Evolution, Molecular, Gene Expression Regulation, HUMANS, Macaca mulatta, Pan troglodytes, Protein Biosynthesis, RNA, Messenger, Selection, Genetic, Species Specificity, Transcription, Genetic}, issn = {1095-9203}, doi = {10.1126/science.1242379}, author = {Khan, Zia and Ford, Michael J and Cusanovich, Darren A and Mitrano, Amy and Pritchard, Jonathan K and Gilad, Yoav} } @article {49545, title = {Primate Transcript and Protein Expression Levels Evolve Under Compensatory Selection Pressures}, volume = {342}, year = {2013}, month = {May-11-2015}, pages = {1100 - 1104}, issn = {0036-8075}, doi = {10.1126/science.1242379}, url = {http://www.sciencemag.org/cgi/doi/10.1126/science.1242379}, author = {Khan, Z. and Ford, M. J. and Cusanovich, D. A. and Mitrano, A. and Pritchard, J. K. and Gilad, Y.} } @article {38509, title = {Somatic alterations contributing to metastasis of a castration-resistant prostate cancer}, journal = {Human mutationHuman mutation}, volume = {34}, year = {2013}, note = {http://www.ncbi.nlm.nih.gov/pubmed/23636849?dopt=Abstract}, type = {10.1002/humu.22346}, abstract = {Metastatic castration-resistant prostate cancer (mCRPC) is a lethal disease, and molecular markers that differentiate indolent from aggressive subtypes are needed. We sequenced the exomes of five metastatic tumors and healthy kidney tissue from an index case with mCRPC to identify lesions associated with disease progression and metastasis. An Ashkenazi Jewish (AJ) germline founder mutation, del185AG in BRCA1, was observed and AJ ancestry was confirmed. Sixty-two somatic variants altered proteins in tumors, including cancer-associated genes, TMPRSS2-ERG, PBRM1, and TET2. The majority (n = 53) of somatic variants were present in all metastases and only a subset (n = 31) was observed in the primary tumor. Integrating tumor next-generation sequencing and DNA copy number showed somatic loss of BRCA1 and TMPRSS2-ERG. We sequenced 19 genes with deleterious mutations in the index case in additional mCRPC samples and detected a frameshift, two somatic missense alterations, tumor loss of heterozygosity, and combinations of germline missense SNPs in TET2. In summary, genetic analysis of metastases from an index case permitted us to infer a chronology for the clonal spread of disease based on sequential accrual of somatic lesions. The role of TET2 in mCRPC deserves additional analysis and may define a subset of metastatic disease.}, author = {Nickerson, Michael L. and Im, Kate M. and Misner, Kevin J. and Tan, Wei and Lou, Hong and Gold, Bert and Wells, David W. and H{\'e}ctor Corrada Bravo and Fredrikson, Karin M. and Harkins, Timothy T. and Milos, Patrice and Zbar, Berton and Linehan, W. Marston and Yeager, Meredith and Andresson, Thorkell and Dean, Michael and Bova, G. Steven} } @article {38195, title = {Deep Sequencing of the Oral Microbiome Reveals Signatures of Periodontal Disease}, journal = {PloS onePLoS One}, volume = {7}, year = {2012}, publisher = {Public Library of Science}, author = {Liu, B. and Faller, L. L. and Klitgord, N. and Mazumdar, V. and Ghodsi, M. and Sommer, D. D. and Gibbons, T. R. and Todd Treangen and Chang, Y. C. and Li, S. and others,} } @article {49774, title = {Genomic insights to SAR86, an abundant and uncultivated marine bacterial lineage.}, journal = {ISME J}, volume = {6}, year = {2012}, month = {2012 Jun}, pages = {1186-99}, abstract = {

Bacteria in the 16S rRNA clade SAR86 are among the most abundant uncultivated constituents of microbial assemblages in the surface ocean for which little genomic information is currently available. Bioinformatic techniques were used to assemble two nearly complete genomes from marine metagenomes and single-cell sequencing provided two more partial genomes. Recruitment of metagenomic data shows that these SAR86 genomes substantially increase our knowledge of non-photosynthetic bacteria in the surface ocean. Phylogenomic analyses establish SAR86 as a basal and divergent lineage of γ-proteobacteria, and the individual genomes display a temperature-dependent distribution. Modestly sized at 1.25-1.7 Mbp, the SAR86 genomes lack several pathways for amino-acid and vitamin synthesis as well as sulfate reduction, trends commonly observed in other abundant marine microbes. SAR86 appears to be an aerobic chemoheterotroph with the potential for proteorhodopsin-based ATP generation, though the apparent lack of a retinal biosynthesis pathway may require it to scavenge exogenously-derived pigments to utilize proteorhodopsin. The genomes contain an expanded capacity for the degradation of lipids and carbohydrates acquired using a wealth of tonB-dependent outer membrane receptors. Like the abundant planktonic marine bacterial clade SAR11, SAR86 exhibits metabolic streamlining, but also a distinct carbon compound specialization, possibly avoiding competition.

}, keywords = {Computational Biology, Gammaproteobacteria, Genome, Bacterial, Genomic Library, metagenomics, Oceans and Seas, Phylogeny, plankton, Rhodopsin, Rhodopsins, Microbial, RNA, Ribosomal, 16S, Seawater}, issn = {1751-7370}, doi = {10.1038/ismej.2011.189}, author = {Dupont, Chris L and Rusch, Douglas B and Yooseph, Shibu and Lombardo, Mary-Jane and Richter, R Alexander and Valas, Ruben and Novotny, Mark and Yee-Greenbaum, Joyclyn and Selengut, Jeremy D and Haft, Dan H and Halpern, Aaron L and Lasken, Roger S and Nealson, Kenneth and Friedman, Robert and Venter, J Craig} } @article {38316, title = {Genomic insights to SAR86, an abundant and uncultivated marine bacterial lineage}, journal = {The ISME journalThe ISME journal}, volume = {6}, year = {2012}, note = {http://www.ncbi.nlm.nih.gov/pubmed/22170421?dopt=Abstract}, type = {10.1038/ismej.2011.189}, abstract = {Bacteria in the 16S rRNA clade SAR86 are among the most abundant uncultivated constituents of microbial assemblages in the surface ocean for which little genomic information is currently available. Bioinformatic techniques were used to assemble two nearly complete genomes from marine metagenomes and single-cell sequencing provided two more partial genomes. Recruitment of metagenomic data shows that these SAR86 genomes substantially increase our knowledge of non-photosynthetic bacteria in the surface ocean. Phylogenomic analyses establish SAR86 as a basal and divergent lineage of γ-proteobacteria, and the individual genomes display a temperature-dependent distribution. Modestly sized at 1.25-1.7 Mbp, the SAR86 genomes lack several pathways for amino-acid and vitamin synthesis as well as sulfate reduction, trends commonly observed in other abundant marine microbes. SAR86 appears to be an aerobic chemoheterotroph with the potential for proteorhodopsin-based ATP generation, though the apparent lack of a retinal biosynthesis pathway may require it to scavenge exogenously-derived pigments to utilize proteorhodopsin. The genomes contain an expanded capacity for the degradation of lipids and carbohydrates acquired using a wealth of tonB-dependent outer membrane receptors. Like the abundant planktonic marine bacterial clade SAR11, SAR86 exhibits metabolic streamlining, but also a distinct carbon compound specialization, possibly avoiding competition.}, keywords = {Computational Biology, Gammaproteobacteria, Genome, Bacterial, Genomic Library, metagenomics, Oceans and Seas, Phylogeny, plankton, Rhodopsin, RNA, Ribosomal, 16S, Seawater}, author = {Dupont, Chris L. and Rusch, Douglas B. and Yooseph, Shibu and Lombardo, Mary-Jane and Richter, R. Alexander and Valas, Ruben and Novotny, Mark and Yee-Greenbaum, Joyclyn and J. Selengut and Haft, Dan H. and Halpern, Aaron L. and Lasken, Roger S. and Nealson, Kenneth and Friedman, Robert and Venter, J. Craig} } @article {38352, title = {InterPro in 2011: new developments in the family and domain prediction database}, journal = {Nucleic acids researchNucleic Acids Research}, volume = {40}, year = {2012}, note = {http://www.ncbi.nlm.nih.gov/pubmed/22096229?dopt=Abstract}, type = {10.1093/nar/gkr948}, abstract = {InterPro (http://www.ebi.ac.uk/interpro/) is a database that integrates diverse information about protein families, domains and functional sites, and makes it freely available to the public via Web-based interfaces and services. Central to the database are diagnostic models, known as signatures, against which protein sequences can be searched to determine their potential function. InterPro has utility in the large-scale analysis of whole genomes and meta-genomes, as well as in characterizing individual protein sequences. Herein we give an overview of new developments in the database and its associated software since 2009, including updates to database content, curation processes and Web and programmatic interfaces.}, keywords = {Databases, Protein, Protein Structure, Tertiary, Proteins, Sequence Analysis, Protein, software, Terminology as Topic, User-Computer Interface}, author = {Hunter, Sarah and Jones, Philip and Mitchell, Alex and Apweiler, Rolf and Attwood, Teresa K. and Bateman, Alex and Bernard, Thomas and Binns, David and Bork, Peer and Burge, Sarah and de Castro, Edouard and Coggill, Penny and Corbett, Matthew and Das, Ujjwal and Daugherty, Louise and Duquenne, Lauranne and Finn, Robert D. and Fraser, Matthew and Gough, Julian and Haft, Daniel and Hulo, Nicolas and Kahn, Daniel and Kelly, Elizabeth and Letunic, Ivica and Lonsdale, David and Lopez, Rodrigo and Madera, Martin and Maslen, John and McAnulla, Craig and McDowall, Jennifer and McMenamin, Conor and Mi, Huaiyu and Mutowo-Muellenet, Prudence and Mulder, Nicola and Natale, Darren and Orengo, Christine and Pesseat, Sebastien and Punta, Marco and Quinn, Antony F. and Rivoire, Catherine and Sangrador-Vegas, Amaia and J. Selengut and Sigrist, Christian J. A. and Scheremetjew, Maxim and Tate, John and Thimmajanarthanan, Manjulapramila and Thomas, Paul D. and Wu, Cathy H. and Yeats, Corin and Yong, Siew-Yit} } @article {49765, title = {InterPro in 2011: new developments in the family and domain prediction database.}, journal = {Nucleic Acids Res}, volume = {40}, year = {2012}, month = {2012 Jan}, pages = {D306-12}, abstract = {

InterPro (http://www.ebi.ac.uk/interpro/) is a database that integrates diverse information about protein families, domains and functional sites, and makes it freely available to the public via Web-based interfaces and services. Central to the database are diagnostic models, known as signatures, against which protein sequences can be searched to determine their potential function. InterPro has utility in the large-scale analysis of whole genomes and meta-genomes, as well as in characterizing individual protein sequences. Herein we give an overview of new developments in the database and its associated software since 2009, including updates to database content, curation processes and Web and programmatic interfaces.

}, keywords = {Databases, Protein, Protein Structure, Tertiary, Proteins, Sequence Analysis, Protein, software, Terminology as Topic, User-Computer Interface}, issn = {1362-4962}, doi = {10.1093/nar/gkr948}, author = {Hunter, Sarah and Jones, Philip and Mitchell, Alex and Apweiler, Rolf and Attwood, Teresa K and Bateman, Alex and Bernard, Thomas and Binns, David and Bork, Peer and Burge, Sarah and de Castro, Edouard and Coggill, Penny and Corbett, Matthew and Das, Ujjwal and Daugherty, Louise and Duquenne, Lauranne and Finn, Robert D and Fraser, Matthew and Gough, Julian and Haft, Daniel and Hulo, Nicolas and Kahn, Daniel and Kelly, Elizabeth and Letunic, Ivica and Lonsdale, David and Lopez, Rodrigo and Madera, Martin and Maslen, John and McAnulla, Craig and McDowall, Jennifer and McMenamin, Conor and Mi, Huaiyu and Mutowo-Muellenet, Prudence and Mulder, Nicola and Natale, Darren and Orengo, Christine and Pesseat, Sebastien and Punta, Marco and Quinn, Antony F and Rivoire, Catherine and Sangrador-Vegas, Amaia and Selengut, Jeremy D and Sigrist, Christian J A and Scheremetjew, Maxim and Tate, John and Thimmajanarthanan, Manjulapramila and Thomas, Paul D and Wu, Cathy H and Yeats, Corin and Yong, Siew-Yit} } @article {49531, title = {Plasmodium falciparum merozoite surface protein 1 blocks the proinflammatory protein S100P.}, volume = {109}, year = {2012}, month = {2012 Apr 3}, pages = {5429-34}, abstract = {

The malaria parasite, Plasmodium falciparum, and the human immune system have coevolved to ensure that the parasite is not eliminated and reinfection is not resisted. This relationship is likely mediated through a myriad of host-parasite interactions, although surprisingly few such interactions have been identified. Here we show that the 33-kDa fragment of P. falciparum merozoite surface protein 1 (MSP1(33)), an abundant protein that is shed during red blood cell invasion, binds to the proinflammatory protein, S100P. MSP1(33) blocks S100P-induced NFκB activation in monocytes and chemotaxis in neutrophils. Remarkably, S100P binds to both dimorphic alleles of MSP1, estimated to have diverged >27 Mya, suggesting an ancient, conserved relationship between these parasite and host proteins that may serve to attenuate potentially damaging inflammatory responses.

}, keywords = {Amino Acid Sequence, Animals, Calcium-Binding Proteins, Chromatography, Gel, Electrophoresis, Polyacrylamide Gel, Enzyme-Linked Immunosorbent Assay, HUMANS, Merozoite Surface Protein 1, Microscopy, Confocal, Molecular Sequence Data, Neoplasm Proteins, Plasmodium falciparum, Sequence Homology, Amino Acid, Surface Plasmon Resonance}, issn = {1091-6490}, doi = {10.1073/pnas.1202689109}, author = {Waisberg, Michael and Cerqueira, Gustavo C and Yager, Stephanie B and Francischetti, Ivo M B and Lu, Jinghua and Gera, Nidhi and Srinivasan, Prakash and Miura, Kazutoyo and Rada, Balazs and Lukszo, Jan and Barbian, Kent D and Leto, Thomas L and Porcella, Stephen F and Narum, David L and El-Sayed, Najib and Miller, Louis H and Pierce, Susan K} } @article {38516, title = {Structure, function and diversity of the healthy human microbiome}, journal = {NatureNature}, volume = {486}, year = {2012}, author = {Huttenhower, C. and Gevers, D. and Knight, R. and Abubucker, S. and Badger, J. H. and Chinwalla, A. T. and Creasy, H. H. and Earl, A. M. and Fitzgerald, M. G. and Fulton, R. S. and others,} } @article {38573, title = {Whole genome analysis of Leptospira licerasiae provides insight into leptospiral evolution and pathogenicity}, journal = {PLoS neglected tropical diseasesPLoS neglected tropical diseases}, volume = {6}, year = {2012}, note = {http://www.ncbi.nlm.nih.gov/pubmed/23145189?dopt=Abstract}, type = {10.1371/journal.pntd.0001853}, abstract = {The whole genome analysis of two strains of the first intermediately pathogenic leptospiral species to be sequenced (Leptospira licerasiae strains VAR010 and MMD0835) provides insight into their pathogenic potential and deepens our understanding of leptospiral evolution. Comparative analysis of eight leptospiral genomes shows the existence of a core leptospiral genome comprising 1547 genes and 452 conserved genes restricted to infectious species (including L. licerasiae) that are likely to be pathogenicity-related. Comparisons of the functional content of the genomes suggests that L. licerasiae retains several proteins related to nitrogen, amino acid and carbohydrate metabolism which might help to explain why these Leptospira grow well in artificial media compared with pathogenic species. L. licerasiae strains VAR010(T) and MMD0835 possess two prophage elements. While one element is circular and shares homology with LE1 of L. biflexa, the second is cryptic and homologous to a previously identified but unnamed region in L. interrogans serovars Copenhageni and Lai. We also report a unique O-antigen locus in L. licerasiae comprised of a 6-gene cluster that is unexpectedly short compared with L. interrogans in which analogous regions may include >90 such genes. Sequence homology searches suggest that these genes were acquired by lateral gene transfer (LGT). Furthermore, seven putative genomic islands ranging in size from 5 to 36 kb are present also suggestive of antecedent LGT. How Leptospira become naturally competent remains to be determined, but considering the phylogenetic origins of the genes comprising the O-antigen cluster and other putative laterally transferred genes, L. licerasiae must be able to exchange genetic material with non-invasive environmental bacteria. The data presented here demonstrate that L. licerasiae is genetically more closely related to pathogenic than to saprophytic Leptospira and provide insight into the genomic bases for its infectiousness and its unique antigenic characteristics.}, keywords = {DNA, Bacterial, Evolution, Molecular, Gene Transfer, Horizontal, Genome, Bacterial, Genomic islands, HUMANS, Leptospira, Molecular Sequence Data, Multigene Family, Prophages, Sequence Analysis, DNA, Virulence factors}, author = {Ricaldi, Jessica N. and Fouts, Derrick E. and J. Selengut and Harkins, Derek M. and Patra, Kailash P. and Moreno, Angelo and Lehmann, Jason S. and Purushe, Janaki and Sanka, Ravi and Torres, Michael and Webster, Nicholas J. and Vinetz, Joseph M. and Matthias, Michael A.} } @article {49776, title = {Whole genome analysis of Leptospira licerasiae provides insight into leptospiral evolution and pathogenicity.}, journal = {PLoS Negl Trop Dis}, volume = {6}, year = {2012}, month = {2012}, pages = {e1853}, abstract = {

The whole genome analysis of two strains of the first intermediately pathogenic leptospiral species to be sequenced (Leptospira licerasiae strains VAR010 and MMD0835) provides insight into their pathogenic potential and deepens our understanding of leptospiral evolution. Comparative analysis of eight leptospiral genomes shows the existence of a core leptospiral genome comprising 1547 genes and 452 conserved genes restricted to infectious species (including L. licerasiae) that are likely to be pathogenicity-related. Comparisons of the functional content of the genomes suggests that L. licerasiae retains several proteins related to nitrogen, amino acid and carbohydrate metabolism which might help to explain why these Leptospira grow well in artificial media compared with pathogenic species. L. licerasiae strains VAR010(T) and MMD0835 possess two prophage elements. While one element is circular and shares homology with LE1 of L. biflexa, the second is cryptic and homologous to a previously identified but unnamed region in L. interrogans serovars Copenhageni and Lai. We also report a unique O-antigen locus in L. licerasiae comprised of a 6-gene cluster that is unexpectedly short compared with L. interrogans in which analogous regions may include >90 such genes. Sequence homology searches suggest that these genes were acquired by lateral gene transfer (LGT). Furthermore, seven putative genomic islands ranging in size from 5 to 36 kb are present also suggestive of antecedent LGT. How Leptospira become naturally competent remains to be determined, but considering the phylogenetic origins of the genes comprising the O-antigen cluster and other putative laterally transferred genes, L. licerasiae must be able to exchange genetic material with non-invasive environmental bacteria. The data presented here demonstrate that L. licerasiae is genetically more closely related to pathogenic than to saprophytic Leptospira and provide insight into the genomic bases for its infectiousness and its unique antigenic characteristics.

}, keywords = {DNA, Bacterial, Evolution, Molecular, Gene Transfer, Horizontal, Genome, Bacterial, Genomic islands, HUMANS, Leptospira, Molecular Sequence Data, Multigene Family, Prophages, Sequence Analysis, DNA, Virulence factors}, issn = {1935-2735}, doi = {10.1371/journal.pntd.0001853}, author = {Ricaldi, Jessica N and Fouts, Derrick E and Selengut, Jeremy D and Harkins, Derek M and Patra, Kailash P and Moreno, Angelo and Lehmann, Jason S and Purushe, Janaki and Sanka, Ravi and Torres, Michael and Webster, Nicholas J and Vinetz, Joseph M and Matthias, Michael A} } @article {38151, title = {Clonal transmission, dual peak, and off-season cholera in Bangladesh}, journal = {Infection Ecology \& EpidemiologyInfection Ecology \& Epidemiology}, volume = {1}, year = {2011}, type = {10.3402/iee.v1i0.7273}, author = {Alam, M. and Islam, A. and Bhuiyan, N. A. and Rahim, N. and Hossain, A. and Khan, G. Y. and Ahmed, D. and Watanabe, H. and Izumiya, H. and Faruque, A. S. G. and Rita R. Colwell} } @article {49854, title = {Complete Columbian mammoth mitogenome suggests interbreeding with woolly mammoths}, journal = {Genome biology}, volume = {12}, year = {2011}, pages = {R51}, author = {Enk, Jacob and Devault, Alison and Debruyne, Regis and King, Christine E and Todd Treangen and O{\textquoteright}Rourke, Dennis and Salzberg, Steven L and Fisher, Daniel and MacPhee, Ross and Poinar, Hendrik} } @article {49727, title = {Haem oxygenase is synthetically lethal with the tumour suppressor fumarate hydratase.}, journal = {Nature}, volume = {477}, year = {2011}, month = {2011 Sep 8}, pages = {225-8}, abstract = {

Fumarate hydratase (FH) is an enzyme of the tricarboxylic acid cycle (TCA cycle) that catalyses the hydration of fumarate into malate. Germline mutations of FH are responsible for hereditary leiomyomatosis and renal-cell cancer (HLRCC). It has previously been demonstrated that the absence of FH leads to the accumulation of fumarate, which activates hypoxia-inducible factors (HIFs) at normal oxygen tensions. However, so far no mechanism that explains the ability of cells to survive without a functional TCA cycle has been provided. Here we use newly characterized genetically modified kidney mouse cells in which Fh1 has been deleted, and apply a newly developed computer model of the metabolism of these cells to predict and experimentally validate a linear metabolic pathway beginning with glutamine uptake and ending with bilirubin excretion from Fh1-deficient cells. This pathway, which involves the biosynthesis and degradation of haem, enables Fh1-deficient cells to use the accumulated TCA cycle metabolites and permits partial mitochondrial NADH production. We predicted and confirmed that targeting this pathway would render Fh1-deficient cells non-viable, while sparing wild-type Fh1-containing cells. This work goes beyond identifying a metabolic pathway that is induced in Fh1-deficient cells to demonstrate that inhibition of haem oxygenation is synthetically lethal when combined with Fh1 deficiency, providing a new potential target for treating HLRCC patients.

}, keywords = {Animals, Bilirubin, Cell Line, Cells, Cultured, Citric Acid Cycle, Computer simulation, Fumarate Hydratase, Fumarates, Genes, Lethal, Genes, Tumor Suppressor, Glutamine, Heme, Heme Oxygenase (Decyclizing), Kidney Neoplasms, Leiomyomatosis, Mice, Mitochondria, Mutation, NAD, Neoplastic Syndromes, Hereditary, Skin Neoplasms, Uterine Neoplasms}, issn = {1476-4687}, doi = {10.1038/nature10363}, author = {Frezza, Christian and Zheng, Liang and Folger, Ori and Rajagopalan, Kartik N and MacKenzie, Elaine D and Jerby, Livnat and Micaroni, Massimo and Chaneton, Barbara and Adam, Julie and Hedley, Ann and Kalna, Gabriela and Tomlinson, Ian P M and Pollard, Patrick J and Watson, Dave G and Deberardinis, Ralph J and Shlomi, Tomer and Ruppin, Eytan and Gottlieb, Eyal} } @article {49831, title = {Increased methylation variation in epigenetic domains across cancer types}, journal = {Nature Genetics}, volume = {43}, year = {2011}, month = {Feb-06-2013}, pages = {768 - 775}, issn = {1061-4036}, doi = {10.1038/ng.865}, url = {http://www.nature.com/doifinder/10.1038/ng.865}, author = {Hansen, Kasper Daniel and Timp, Winston and Bravo, H{\'e}ctor Corrada and Sabunciyan, Sarven and Langmead, Benjamin and McDonald, Oliver G and Wen, Bo and Wu, Hao and Liu, Yun and Diep, Dinh and Briem, Eirikur and Zhang, Kun and Irizarry, Rafael A and Feinberg, Andrew P} } @article {49830, title = {A Model for Early Prediction of Facial Nerve Recovery After Vestibular Schwannoma Surgery}, journal = {Otology \& Neurotology}, volume = {32}, year = {2011}, month = {Jan-01-2011}, pages = {826 - 833}, issn = {1531-7129}, doi = {10.1097/MAO.0b013e31821b0afd}, url = {http://content.wkhealth.com/linkback/openurl?sid=WKPTLP:landingpage\&an=00129492-201107000-00019}, author = {Rivas, Alejandro and Boahene, Kofi D. and Bravo, H{\'e}ctor Corrada and Tan, Marietta and Tamargo, Rafael J. and Francis, Howard W.} } @article {49728, title = {Predicting selective drug targets in cancer through metabolic networks.}, journal = {Mol Syst Biol}, volume = {7}, year = {2011}, month = {2011}, pages = {501}, abstract = {

The interest in studying metabolic alterations in cancer and their potential role as novel targets for therapy has been rejuvenated in recent years. Here, we report the development of the first genome-scale network model of cancer metabolism, validated by correctly identifying genes essential for cellular proliferation in cancer cell lines. The model predicts 52 cytostatic drug targets, of which 40\% are targeted by known, approved or experimental anticancer drugs, and the rest are new. It further predicts combinations of synthetic lethal drug targets, whose synergy is validated using available drug efficacy and gene expression measurements across the NCI-60 cancer cell line collection. Finally, potential selective treatments for specific cancers that depend on cancer type-specific downregulation of gene expression and somatic mutations are compiled.

}, keywords = {Cell Line, Tumor, Cell Proliferation, Computational Biology, Cytostatic Agents, Down-Regulation, Drug Delivery Systems, Gene Expression Regulation, Neoplastic, HUMANS, Metabolic Networks and Pathways, Models, Biological, Neoplasms, RNA, Small Interfering}, issn = {1744-4292}, doi = {10.1038/msb.2011.35}, author = {Folger, Ori and Jerby, Livnat and Frezza, Christian and Gottlieb, Eyal and Ruppin, Eytan and Shlomi, Tomer} } @article {38470, title = {A robust and rotationally invariant local surface descriptor with applications to non-local mesh processing}, journal = {Graphical ModelsGraphical Models}, volume = {73}, year = {2011}, type = {10.1016/j.gmod.2011.05.002}, abstract = {In recent years, we have witnessed a striking increase in research concerning how to describe a meshed surface. These descriptors are commonly used to encode mesh properties or guide mesh processing, not to augment existing computations by replication. In this work, we first define a robust surface descriptor based on a local height field representation, and present a transformation via the extraction of Zernike moments. Unlike previous work, our local surface descriptor is innately rotationally invariant. Second, equipped with this novel descriptor, we present SAMPLE {\textendash} similarity augmented mesh processing using local exemplars {\textendash} a method which uses feature neighbourhoods to propagate mesh processing done in one part of the mesh, the local exemplar, to many others. Finally, we show that SAMPLE can be used in a number of applications, such as detail transfer and parameterization.}, keywords = {Local descriptors, Non-local mesh processing, shape analysis, Similarity processing}, isbn = {1524-0703}, author = {Maximo, A. and Patro, R. and Varshney, Amitabh and Farias, R.} } @article {38518, title = {Suppression subtractive hybridization PCR isolation of cDNAs from a Caribbean soft coral}, journal = {Electronic Journal of BiotechnologyElectronic Journal of Biotechnology}, volume = {14}, year = {2011}, publisher = {SciELO Chile}, author = {Lopez, J. V. and Ledger, A. and Santiago-V{\'a}zquez, L. Z. and M. Pop and Sommer, D. D. and Ranzer, L. K. and Feldman, R. A. and Russell, G. K.} } @article {38568, title = {Vibrio Cholerae O1 Detection in Estuarine and Coastal Zooplankton}, journal = {Journal of Plankton ResearchJ. Plankton Res.Journal of Plankton ResearchJ. Plankton Res.}, volume = {33}, year = {2011}, type = {10.1093/plankt/fbq093}, abstract = {Vibrio cholerae is an autochthonous marine bacterium, and its association with diverse planktonic crustaceans has been extensively investigated; however, the presence of V. cholerae on individuals of most phyla of planktonic animals is still incompletely understood. The objective of this study was to analyze the distribution of V. cholerae serogroup O1 associated with specific zooplankton taxa in an estuary and the adjacent continental shelf of the southeastern Brazilian coast. The occurrence of the bacterium was assessed in zooplankton samples, specifically on the most abundant taxa, using direct fluorescence assay (DFA) and direct viable count{\textendash}direct fluorescence assay (DVC{\textendash}DFA) methods. Vibrio cholerae O1 was detected in 88\% of samples collected from the Santos-Bertioga estuary and in 67\% of samples from the shelf. The salinity of the estuarine water ranged from 21.8 to 34.6, significantly lower than the shelf water which was 32.1{\textendash}36.1. Salinity was the only environmental variable measured that displayed a significant correlation with the presence of V. cholerae (P< 0.05). Vibrio cholerae O1 was detected in chaetognaths, pluteus larvae of echinoderms and planktonic fish eggs (Engraulidae), all new sites for this bacterium.}, keywords = {DFA, estuary, plankton, Southwest Atlantic}, isbn = {0142-7873, 1464-3774}, author = {Martinelli Filho, Jos{\'e} E. and Lopes, Rubens M. and Rivera, Irma N. G. and Rita R. Colwell} } @article {49648, title = {The Alveolate Perkinsus marinus: biological insights from EST gene discovery.}, journal = {BMC Genomics}, volume = {11}, year = {2010}, month = {2010}, pages = {228}, abstract = {

BACKGROUND: Perkinsus marinus, a protozoan parasite of the eastern oyster Crassostrea virginica, has devastated natural and farmed oyster populations along the Atlantic and Gulf coasts of the United States. It is classified as a member of the Perkinsozoa, a recently established phylum considered close to the ancestor of ciliates, dinoflagellates, and apicomplexans, and a key taxon for understanding unique adaptations (e.g. parasitism) within the Alveolata. Despite intense parasite pressure, no disease-resistant oysters have been identified and no effective therapies have been developed to date.

RESULTS: To gain insight into the biological basis of the parasite{\textquoteright}s virulence and pathogenesis mechanisms, and to identify genes encoding potential targets for intervention, we generated>31,000 5{\textquoteright} expressed sequence tags (ESTs) derived from four trophozoite libraries generated from two P. marinus strains. Trimming and clustering of the sequence tags yielded 7,863 unique sequences, some of which carry a spliced leader. Similarity searches revealed that 55\% of these had hits in protein sequence databases, of which 1,729 had their best hit with proteins from the chromalveolates (E-value

CONCLUSIONS: Our transcriptome analysis of P. marinus, the first for any member of the Perkinsozoa, contributes new insight into its biology and taxonomic position. It provides a very informative, albeit preliminary, glimpse into the expression of genes encoding functionally relevant proteins as potential targets for chemotherapy, and evidence for the presence of a relict plastid. Further, although P. marinus sequences display significant similarity to those from both apicomplexans and dinoflagellates, the presence of trans-spliced transcripts confirms the previously established affinities with the latter. The EST analysis reported herein, together with the recently completed sequence of the P. marinus genome and the development of transfection methodology, should result in improved intervention strategies against dermo disease.

}, keywords = {Alveolata, Animals, Expressed Sequence Tags, Ostreidae, Phylogeny}, issn = {1471-2164}, doi = {10.1186/1471-2164-11-228}, author = {Joseph, Sandeep J and Fern{\'a}ndez-Robledo, Jos{\'e} A and Gardner, Malcolm J and El-Sayed, Najib M and Kuo, Chih-Horng and Schott, Eric J and Wang, Haiming and Kissinger, Jessica C and Vasta, Gerardo R} } @article {49650, title = {A model for using a concept inventory as a tool for students{\textquoteright} assessment and faculty professional development.}, journal = {CBE Life Sci Educ}, volume = {9}, year = {2010}, month = {2010 Winter}, pages = {408-16}, abstract = {

This essay describes how the use of a concept inventory has enhanced professional development and curriculum reform efforts of a faculty teaching community. The Host Pathogen Interactions (HPI) teaching team is composed of research and teaching faculty with expertise in HPI who share the goal of improving the learning experience of students in nine linked undergraduate microbiology courses. To support evidence-based curriculum reform, we administered our HPI Concept Inventory as a pre- and postsurvey to approximately 400 students each year since 2006. The resulting data include student scores as well as their open-ended explanations for distractor choices. The data have enabled us to address curriculum reform goals of 1) reconciling student learning with our expectations, 2) correlating student learning with background variables, 3) understanding student learning across institutions, 4) measuring the effect of teaching techniques on student learning, and 5) demonstrating how our courses collectively form a learning progression. The analysis of the concept inventory data has anchored and deepened the team{\textquoteright}s discussions of student learning. Reading and discussing students{\textquoteright} responses revealed the gap between our understanding and the students{\textquoteright} understanding. We provide evidence to support the concept inventory as a tool for assessing student understanding of HPI concepts and faculty development.

}, keywords = {Curriculum, Faculty, Models, Theoretical, Research, Students, Teaching}, issn = {1931-7913}, doi = {10.1187/cbe.10-05-0069}, author = {Marbach-Ad, Gili and McAdams, Katherine C and Benson, Spencer and Briken, Volker and Cathcart, Laura and Chase, Michael and El-Sayed, Najib M and Frauwirth, Kenneth and Fredericksen, Brenda and Joseph, Sam W and Lee, Vincent and McIver, Kevin S and Mosser, David and Quimby, B Booth and Shields, Patricia and Song, Wenxia and Stein, Daniel C and Stewart, Richard and Thompson, Katerina V and Smith, Ann C} } @article {49645, title = {Assessing Student Understanding of Host Pathogen Interactions Using a Concept Inventory}, journal = {J. Microbiol. Biol. Ed.}, volume = {10}, year = {2009}, pages = {43-50}, author = {Marbach-Ad, G. and Briken, V. and El-Sayed, N.M. and Frauwirth, K. and Fredericksen, B. and Hutcheson, S. and Gao, L.-Y. and Joseph, S. and Lee, V. and McIver, K.S. and Mosser, D. and Quimby, B.B. and Shields, P. and Song, W. and Stein, D.C. and Yuan, R.T. and Smith, A.C.} } @article {38167, title = {Complete Genome Sequence of Aggregatibacter (Haemophilus) Aphrophilus NJ8700}, journal = {Journal of BacteriologyJ. Bacteriol.Journal of BacteriologyJ. Bacteriol.}, volume = {191}, year = {2009}, type = {10.1128/JB.00447-09}, abstract = {We report the finished and annotated genome sequence of Aggregatibacter aphrophilus strain NJ8700, a strain isolated from the oral flora of a healthy individual, and discuss characteristics that may affect its dual roles in human health and disease. This strain has a rough appearance, and its genome contains genes encoding a type VI secretion system and several factors that may participate in host colonization.}, isbn = {0021-9193, 1098-5530}, author = {Di Bonaventura, Maria Pia and DeSalle, Rob and M. Pop and Nagarajan, Niranjan and Figurski, David H. and Fine, Daniel H. and Kaplan, Jeffrey B. and Planet, Paul J.} } @article {49646, title = {The genome of the blood fluke Schistosoma mansoni.}, journal = {Nature}, volume = {460}, year = {2009}, month = {2009 Jul 16}, pages = {352-8}, abstract = {

Schistosoma mansoni is responsible for the neglected tropical disease schistosomiasis that affects 210 million people in 76 countries. Here we present analysis of the 363 megabase nuclear genome of the blood fluke. It encodes at least 11,809 genes, with an unusual intron size distribution, and new families of micro-exon genes that undergo frequent alternative splicing. As the first sequenced flatworm, and a representative of the Lophotrochozoa, it offers insights into early events in the evolution of the animals, including the development of a body pattern with bilateral symmetry, and the development of tissues into organs. Our analysis has been informed by the need to find new drug targets. The deficits in lipid metabolism that make schistosomes dependent on the host are revealed, and the identification of membrane receptors, ion channels and more than 300 proteases provide new insights into the biology of the life cycle and new targets. Bioinformatics approaches have identified metabolic chokepoints, and a chemogenomic screen has pinpointed schistosome proteins for which existing drugs may be active. The information generated provides an invaluable resource for the research community to develop much needed new control tools for the treatment and eradication of this important and neglected disease.

}, keywords = {Animals, Biological Evolution, Exons, Genes, Helminth, Genome, Helminth, Host-Parasite Interactions, Introns, Molecular Sequence Data, Physical Chromosome Mapping, Schistosoma mansoni, Schistosomiasis mansoni}, issn = {1476-4687}, doi = {10.1038/nature08160}, author = {Berriman, Matthew and Haas, Brian J and LoVerde, Philip T and Wilson, R Alan and Dillon, Gary P and Cerqueira, Gustavo C and Mashiyama, Susan T and Al-Lazikani, Bissan and Andrade, Luiza F and Ashton, Peter D and Aslett, Martin A and Bartholomeu, Daniella C and Blandin, Ga{\"e}lle and Caffrey, Conor R and Coghlan, Avril and Coulson, Richard and Day, Tim A and Delcher, Art and DeMarco, Ricardo and Djikeng, Appolinaire and Eyre, Tina and Gamble, John A and Ghedin, Elodie and Gu, Yong and Hertz-Fowler, Christiane and Hirai, Hirohisha and Hirai, Yuriko and Houston, Robin and Ivens, Alasdair and Johnston, David A and Lacerda, Daniela and Macedo, Camila D and McVeigh, Paul and Ning, Zemin and Oliveira, Guilherme and Overington, John P and Parkhill, Julian and Pertea, Mihaela and Pierce, Raymond J and Protasio, Anna V and Quail, Michael A and Rajandream, Marie-Ad{\`e}le and Rogers, Jane and Sajid, Mohammed and Salzberg, Steven L and Stanke, Mario and Tivey, Adrian R and White, Owen and Williams, David L and Wortman, Jennifer and Wu, Wenjie and Zamanian, Mostafa and Zerlotini, Adhemar and Fraser-Liggett, Claire M and Barrell, Barclay G and El-Sayed, Najib M} } @article {49781, title = {InterPro: the integrative protein signature database.}, journal = {Nucleic Acids Res}, volume = {37}, year = {2009}, month = {2009 Jan}, pages = {D211-5}, abstract = {

The InterPro database (http://www.ebi.ac.uk/interpro/) integrates together predictive models or {\textquoteright}signatures{\textquoteright} representing protein domains, families and functional sites from multiple, diverse source databases: Gene3D, PANTHER, Pfam, PIRSF, PRINTS, ProDom, PROSITE, SMART, SUPERFAMILY and TIGRFAMs. Integration is performed manually and approximately half of the total approximately 58,000 signatures available in the source databases belong to an InterPro entry. Recently, we have started to also display the remaining un-integrated signatures via our web interface. Other developments include the provision of non-signature data, such as structural data, in new XML files on our FTP site, as well as the inclusion of matchless UniProtKB proteins in the existing match XML files. The web interface has been extended and now links out to the ADAN predicted protein-protein interaction database and the SPICE and Dasty viewers. The latest public release (v18.0) covers 79.8\% of UniProtKB (v14.1) and consists of 16 549 entries. InterPro data may be accessed either via the web address above, via web services, by downloading files by anonymous FTP or by using the InterProScan search software (http://www.ebi.ac.uk/Tools/InterProScan/).

}, keywords = {Databases, Protein, Proteins, Sequence Analysis, Protein, Systems Integration}, issn = {1362-4962}, doi = {10.1093/nar/gkn785}, author = {Hunter, Sarah and Apweiler, Rolf and Attwood, Teresa K and Bairoch, Amos and Bateman, Alex and Binns, David and Bork, Peer and Das, Ujjwal and Daugherty, Louise and Duquenne, Lauranne and Finn, Robert D and Gough, Julian and Haft, Daniel and Hulo, Nicolas and Kahn, Daniel and Kelly, Elizabeth and Laugraud, Aur{\'e}lie and Letunic, Ivica and Lonsdale, David and Lopez, Rodrigo and Madera, Martin and Maslen, John and McAnulla, Craig and McDowall, Jennifer and Mistry, Jaina and Mitchell, Alex and Mulder, Nicola and Natale, Darren and Orengo, Christine and Quinn, Antony F and Selengut, Jeremy D and Sigrist, Christian J A and Thimma, Manjula and Thomas, Paul D and Valentin, Franck and Wilson, Derek and Wu, Cathy H and Yeats, Corin} } @article {38353, title = {InterPro: the integrative protein signature database}, journal = {Nucleic acids researchNucleic Acids Research}, volume = {37}, year = {2009}, note = {http://www.ncbi.nlm.nih.gov/pubmed/18940856?dopt=Abstract}, type = {10.1093/nar/gkn785}, abstract = {The InterPro database (http://www.ebi.ac.uk/interpro/) integrates together predictive models or {\textquoteright}signatures{\textquoteright} representing protein domains, families and functional sites from multiple, diverse source databases: Gene3D, PANTHER, Pfam, PIRSF, PRINTS, ProDom, PROSITE, SMART, SUPERFAMILY and TIGRFAMs. Integration is performed manually and approximately half of the total approximately 58,000 signatures available in the source databases belong to an InterPro entry. Recently, we have started to also display the remaining un-integrated signatures via our web interface. Other developments include the provision of non-signature data, such as structural data, in new XML files on our FTP site, as well as the inclusion of matchless UniProtKB proteins in the existing match XML files. The web interface has been extended and now links out to the ADAN predicted protein-protein interaction database and the SPICE and Dasty viewers. The latest public release (v18.0) covers 79.8\% of UniProtKB (v14.1) and consists of 16 549 entries. InterPro data may be accessed either via the web address above, via web services, by downloading files by anonymous FTP or by using the InterProScan search software (http://www.ebi.ac.uk/Tools/InterProScan/).}, keywords = {Databases, Protein, Proteins, Sequence Analysis, Protein, Systems Integration}, author = {Hunter, Sarah and Apweiler, Rolf and Attwood, Teresa K. and Bairoch, Amos and Bateman, Alex and Binns, David and Bork, Peer and Das, Ujjwal and Daugherty, Louise and Duquenne, Lauranne and Finn, Robert D. and Gough, Julian and Haft, Daniel and Hulo, Nicolas and Kahn, Daniel and Kelly, Elizabeth and Laugraud, Aur{\'e}lie and Letunic, Ivica and Lonsdale, David and Lopez, Rodrigo and Madera, Martin and Maslen, John and McAnulla, Craig and McDowall, Jennifer and Mistry, Jaina and Mitchell, Alex and Mulder, Nicola and Natale, Darren and Orengo, Christine and Quinn, Antony F. and J. Selengut and Sigrist, Christian J. A. and Thimma, Manjula and Thomas, Paul D. and Valentin, Franck and Wilson, Derek and Wu, Cathy H. and Yeats, Corin} } @article {38559, title = {Using Satellite Images of Environmental Changes to Predict Infectious Disease Outbreaks}, journal = {Emerging Infectious DiseasesEmerg Infect DisEmerging Infectious DiseasesEmerg Infect Dis}, volume = {15}, year = {2009}, type = {10.3201/eid/1509.081334}, abstract = {A strong global satellite imaging system is essential for predicting outbreaks., Recent events clearly illustrate a continued vulnerability of large populations to infectious diseases, which is related to our changing human-constructed and natural environments. A single person with multidrug-resistant tuberculosis in 2007 provided a wake-up call to the United States and global public health infrastructure, as the health professionals and the public realized that today{\textquoteright}s ease of airline travel can potentially expose hundreds of persons to an untreatable disease associated with an infectious agent. Ease of travel, population increase, population displacement, pollution, agricultural activity, changing socioeconomic structures, and international conflicts worldwide have each contributed to infectious disease events. Today, however, nothing is larger in scale, has more potential for long-term effects, and is more uncertain than the effects of climate change on infectious disease outbreaks, epidemics, and pandemics. We discuss advances in our ability to predict these events and, in particular, the critical role that satellite imaging could play in mounting an effective response.}, isbn = {1080-6040}, author = {Ford, Timothy E. and Rita R. Colwell and Rose, Joan B. and Morse, Stephen S. and Rogers, David J. and Yates, Terry L.} } @article {49676, title = {The draft genome of the transgenic tropical fruit tree papaya (Carica papaya Linnaeus).}, journal = {Nature}, volume = {452}, year = {2008}, month = {2008 Apr 24}, pages = {991-6}, abstract = {

Papaya, a fruit crop cultivated in tropical and subtropical regions, is known for its nutritional benefits and medicinal applications. Here we report a 3x draft genome sequence of {\textquoteright}SunUp{\textquoteright} papaya, the first commercial virus-resistant transgenic fruit tree to be sequenced. The papaya genome is three times the size of the Arabidopsis genome, but contains fewer genes, including significantly fewer disease-resistance gene analogues. Comparison of the five sequenced genomes suggests a minimal angiosperm gene set of 13,311. A lack of recent genome duplication, atypical of other angiosperm genomes sequenced so far, may account for the smaller papaya gene number in most functional groups. Nonetheless, striking amplifications in gene number within particular functional groups suggest roles in the evolution of tree-like habit, deposition and remobilization of starch reserves, attraction of seed dispersal agents, and adaptation to tropical daylengths. Transgenesis at three locations is closely associated with chloroplast insertions into the nuclear genome, and with topoisomerase I recognition sites. Papaya offers numerous advantages as a system for fruit-tree functional genomics, and this draft genome sequence provides the foundation for revealing the basis of Carica{\textquoteright}s distinguishing morpho-physiological, medicinal and nutritional properties.

}, keywords = {Arabidopsis, Carica, Contig Mapping, Databases, Genetic, Genes, Plant, Genome, Plant, Molecular Sequence Data, Plants, Genetically Modified, sequence alignment, Sequence Analysis, DNA, Transcription Factors, Tropical Climate}, issn = {1476-4687}, doi = {10.1038/nature06856}, author = {Ming, Ray and Hou, Shaobin and Feng, Yun and Yu, Qingyi and Dionne-Laporte, Alexandre and Saw, Jimmy H and Senin, Pavel and Wang, Wei and Ly, Benjamin V and Lewis, Kanako L T and Salzberg, Steven L and Feng, Lu and Jones, Meghan R and Skelton, Rachel L and Murray, Jan E and Chen, Cuixia and Qian, Wubin and Shen, Junguo and Du, Peng and Eustice, Moriah and Tong, Eric and Tang, Haibao and Lyons, Eric and Paull, Robert E and Michael, Todd P and Wall, Kerr and Rice, Danny W and Albert, Henrik and Wang, Ming-Li and Zhu, Yun J and Schatz, Michael and Nagarajan, Niranjan and Acob, Ricelle A and Guan, Peizhu and Blas, Andrea and Wai, Ching Man and Ackerman, Christine M and Ren, Yan and Liu, Chao and Wang, Jianmei and Wang, Jianping and Na, Jong-Kuk and Shakirov, Eugene V and Haas, Brian and Thimmapuram, Jyothi and Nelson, David and Wang, Xiyin and Bowers, John E and Gschwend, Andrea R and Delcher, Arthur L and Singh, Ratnesh and Suzuki, Jon Y and Tripathi, Savarni and Neupane, Kabi and Wei, Hairong and Irikura, Beth and Paidi, Maya and Jiang, Ning and Zhang, Wenli and Presting, Gernot and Windsor, Aaron and Navajas-P{\'e}rez, Rafael and Torres, Manuel J and Feltus, F Alex and Porter, Brad and Li, Yingjun and Burroughs, A Max and Luo, Ming-Cheng and Liu, Lei and Christopher, David A and Mount, Stephen M and Moore, Paul H and Sugimura, Tak and Jiang, Jiming and Schuler, Mary A and Friedman, Vikki and Mitchell-Olds, Thomas and Shippen, Dorothy E and dePamphilis, Claude W and Palmer, Jeffrey D and Freeling, Michael and Paterson, Andrew H and Gonsalves, Dennis and Wang, Lei and Alam, Maqsudul} } @article {38366, title = {Maternal depletion of CTCF reveals multiple functions during oocyte and preimplantation embryo development}, journal = {DevelopmentDevelopment}, volume = {135}, year = {2008}, publisher = {The Company of Biologists Limited}, author = {Wan, L. B. and Pan, H. and Sridhar Hannenhalli and Cheng, Y. and Ma, J. and Fedoriw, A. and Lobanenkov, V. and Latham, K. E. and Schultz, R. M. and Bartolomei, M. S.} } @article {38383, title = {The minimum information about a genome sequence (MIGS) specification}, journal = {Nature biotechnologyNature biotechnology}, volume = {26}, year = {2008}, note = {http://www.ncbi.nlm.nih.gov/pubmed/18464787?dopt=Abstract}, type = {10.1038/nbt1360}, abstract = {With the quantity of genomic data increasing at an exponential rate, it is imperative that these data be captured electronically, in a standard format. Standardization activities must proceed within the auspices of open-access and international working bodies. To tackle the issues surrounding the development of better descriptions of genomic investigations, we have formed the Genomic Standards Consortium (GSC). Here, we introduce the minimum information about a genome sequence (MIGS) specification with the intent of promoting participation in its development and discussing the resources that will be required to develop improved mechanisms of metadata capture and exchange. As part of its wider goals, the GSC also supports improving the {\textquoteright}transparency{\textquoteright} of the information contained in existing genomic databases.}, keywords = {Chromosome mapping, Databases, Factual, information dissemination, Information Storage and Retrieval, Information Theory, Internationality}, author = {Field, Dawn and Garrity, George and Gray, Tanya and Morrison, Norman and J. Selengut and Sterk, Peter and Tatusova, Tatiana and Thomson, Nicholas and Allen, Michael J. and Angiuoli, Samuel V. and Ashburner, Michael and Axelrod, Nelson and Baldauf, Sandra and Ballard, Stuart and Boore, Jeffrey and Cochrane, Guy and Cole, James and Dawyndt, Peter and De Vos, Paul and DePamphilis, Claude and Edwards, Robert and Faruque, Nadeem and Feldman, Robert and Gilbert, Jack and Gilna, Paul and Gl{\"o}ckner, Frank Oliver and Goldstein, Philip and Guralnick, Robert and Haft, Dan and Hancock, David and Hermjakob, Henning and Hertz-Fowler, Christiane and Hugenholtz, Phil and Joint, Ian and Kagan, Leonid and Kane, Matthew and Kennedy, Jessie and Kowalchuk, George and Kottmann, Renzo and Kolker, Eugene and Kravitz, Saul and Kyrpides, Nikos and Leebens-Mack, Jim and Lewis, Suzanna E. and Li, Kelvin and Lister, Allyson L. and Lord, Phillip and Maltsev, Natalia and Markowitz, Victor and Martiny, Jennifer and Methe, Barbara and Mizrachi, Ilene and Moxon, Richard and Nelson, Karen and Parkhill, Julian and Proctor, Lita and White, Owen and Sansone, Susanna-Assunta and Spiers, Andrew and Stevens, Robert and Swift, Paul and Taylor, Chris and Tateno, Yoshio and Tett, Adrian and Turner, Sarah and Ussery, David and Vaughan, Bob and Ward, Naomi and Whetzel, Trish and San Gil, Ingio and Wilson, Gareth and Wipat, Anil} } @article {49643, title = {Schistosoma mansoni: Microarray analysis of gene expression induced by host sex.}, journal = {Exp Parasitol}, volume = {120}, year = {2008}, month = {2008 Dec}, pages = {357-63}, abstract = {

Schistosoma mansoni is a digenetic trematode and a human parasite responsible for high social and economic impact. Although some authors have studied the effect of host hormones on parasites, not much is known about the effects of host sex on gene expression in Schistosomes. In order to study gene transcripts associated with the host sex, we compared the gene expression profiles of both male and female unisexual adult S. mansoni parasites raised on either male or female hosts, using DNA microarrays. Our results show that host sex caused differential expression of at least 11 genes in female parasites and of 134 in male parasites. Of the differentially expressed genes in female worms, 10 were preferentially expressed in female worms from male mice, while of the 134 differentially expressed genes in male parasites, 79 (59\%) were preferentially expressed in worms from female mice. Further investigation of the role of each of those genes will help understand better their importance in the pathogenesis of Schistosomiasis.

}, keywords = {Animals, Biomphalaria, Female, Gene expression, Host-Parasite Interactions, Male, Mice, Oligonucleotide Array Sequence Analysis, Reverse Transcriptase Polymerase Chain Reaction, RNA, Helminth, Schistosoma mansoni, Schistosomiasis mansoni, Sex Factors}, issn = {1090-2449}, doi = {10.1016/j.exppara.2008.09.005}, author = {Waisberg, M and Lobo, F P and Cerqueira, G C and Passos, L K J and Carvalho, O S and El-Sayed, N M and Franco, G R} } @article {38484, title = {Seasonal Cholera from Multiple Small Outbreaks, Rural Bangladesh}, journal = {Emerging Infectious DiseasesEmerg Infect DisEmerging Infectious DiseasesEmerg Infect Dis}, volume = {14}, year = {2008}, type = {10.3201/eid1405.071116}, abstract = {Clinical and environmental Vibrio cholerae organisms collected from February 2004 through April 2005 were systematically isolated from 2 rural Bangladeshi locales. Their genetic relatedness was evaluated at 5 loci that contained a variable number of tandem repeats (VNTR). The observed minimal overlap in VNTR patterns between the 2 communities was consistent with sequential, small outbreaks from local sources.}, isbn = {1080-6040}, author = {Stine, O. Colin and Alam, Munirul and Tang, Li and Nair, G. Balakrish and Siddique, A. Kasem and Faruque, Shah M. and Huq, Anwar and Rita R. Colwell and Sack, R. Bradley and Morris, J. Glenn} } @article {38491, title = {Sequence diversity and evolution of multigene families in Trypanosoma cruzi}, journal = {Molecular and Biochemical ParasitologyMolecular and Biochemical Parasitology}, volume = {157}, year = {2008}, type = {16/j.molbiopara.2007.10.002}, abstract = {Several copies of genes belonging to three multigene families present in the genome of Trypanosoma cruzi were sequenced and comparatively analyzed across six different strains of the parasite belonging to the T. cruzi I lineage (Colombiana, Silvio X10 and Dm28c), the T. cruzi II lineage (Esmeraldo and JG) and a hybrid strain (CL Brener). For all three gene families analyzed, our results support the division in T. cruzi I and II lineages. Furthermore, in agreement with its hybrid nature, sequences derived from the CL Brener clone clustered together with T. cruzi II sequences as well as with a third group of sequences. Paralogous sequences encoding Amastin, an amastigote surface glycoprotein and TcAG48, an antigenic RNA binding protein, which are clustered in the parasite genome, present higher intragenomic variability in T. cruzi II and CL Brener strains, when compared to T. cruzi I strains. Paralogous sequences derived from the TcADC gene family, which encode various isoforms of adenylyl cyclases and are dispersed throughout the T. cruzi genome, exhibit similar degree of variability in all strains, except in the CL Brener strain, in which the sequences were more divergent. Several factors including mutation rates and gene conversion mechanisms, acting differently within the T. cruzi population, may contribute to create such distinct levels of sequence diversity in multigene families that are clustered in the T. cruzi genome.}, keywords = {Amastin, Gene conversion, Genetic diversity, Multigene families, Trypanosoma cruzi}, isbn = {0166-6851}, author = {Cerqueira, Gustavo C. and Bartholomeu, Daniella C. and DaRocha, Wanderson D. and Hou, Lihua and Freitas-Silva, Danielle M. and Machado, Carlos Renato and Najib M. El-Sayed and Teixeira, Santuza M. R.} } @article {38499, title = {Sex and age dimorphism of myocardial gene expression in nonischemic human heart failure}, journal = {Circulation: Cardiovascular GeneticsCirculation: Cardiovascular Genetics}, volume = {1}, year = {2008}, publisher = {Am Heart Assoc}, author = {Fermin, D. R. and Barac, A. and Lee, S. and Polster, S. P. and Sridhar Hannenhalli and Bergemann, T. L. and Grindle, S. and Dyke, D. B. and Pagani, F. and Miller, L. W. and others,} } @article {38152, title = {Cofactor-independent phosphoglycerate mutase is an essential gene in procyclic form Trypanosoma brucei}, journal = {Parasitology researchParasitology research}, volume = {100}, year = {2007}, author = {Djikeng, A. and Raverdy, S. and Foster, Jeffrey S. and Bartholomeu, D. and Zhang, Y. and Najib M. El-Sayed and Carlow, C.} } @article {38242, title = {Evolution of genes and genomes on the Drosophila phylogeny}, journal = {NatureNature}, volume = {450}, year = {2007}, note = {[szlig]}, type = {10.1038/nature06341}, abstract = {Comparative analysis of multiple genomes in a phylogenetic framework dramatically improves the precision and sensitivity of evolutionary inference, producing more robust results than single-genome analyses can provide. The genomes of 12 Drosophila species, ten of which are presented here for the first time (sechellia, simulans, yakuba, erecta, ananassae, persimilis, willistoni, mojavensis, virilis and grimshawi), illustrate how rates and patterns of sequence divergence across taxa can illuminate evolutionary processes on a genomic scale. These genome sequences augment the formidable genetic tools that have made Drosophila melanogaster a pre-eminent model for animal genetics, and will further catalyse fundamental research on mechanisms of development, cell biology, genetics, disease, neurobiology, behaviour, physiology and evolution. Despite remarkable similarities among these Drosophila species, we identified many putatively non-neutral changes in protein-coding genes, non-coding RNA genes, and cis-regulatory regions. These may prove to underlie differences in the ecology and behaviour of these diverse species.}, isbn = {0028-0836}, author = {Clark, Andrew G. and Eisen, Michael B. and Smith, Douglas R. and Bergman, Casey M. and Oliver, Brian and Markow, Therese A. and Kaufman, Thomas C. and Kellis, Manolis and Gelbart, William and Iyer, Venky N. and Pollard, Daniel A. and Sackton, Timothy B. and Larracuente, Amanda M. and Singh, Nadia D. and Abad, Jose P. and Abt, Dawn N. and Adryan, Boris and Aguade, Montserrat and Akashi, Hiroshi and Anderson, Wyatt W. and Aquadro, Charles F. and Ardell, David H. and Arguello, Roman and Artieri, Carlo G. and Barbash, Daniel A. and Barker, Daniel and Barsanti, Paolo and Batterham, Phil and Batzoglou, Serafim and Begun, Dave and Bhutkar, Arjun and Blanco, Enrico and Bosak, Stephanie A. and Bradley, Robert K. and Brand, Adrianne D. and Brent, Michael R. and Brooks, Angela N. and Brown, Randall H. and Butlin, Roger K. and Caggese, Corrado and Calvi, Brian R. and Carvalho, A. Bernardo de and Caspi, Anat and Castrezana, Sergio and Celniker, Susan E. and Chang, Jean L. and Chapple, Charles and Chatterji, Sourav and Chinwalla, Asif and Civetta, Alberto and Clifton, Sandra W. and Comeron, Josep M. and Costello, James C. and Coyne, Jerry A. and Daub, Jennifer and David, Robert G. and Delcher, Arthur L. and Delehaunty, Kim and Do, Chuong B. and Ebling, Heather and Edwards, Kevin and Eickbush, Thomas and Evans, Jay D. and Filipski, Alan and Findei, and Sven and Freyhult, Eva and Fulton, Lucinda and Fulton, Robert and Garcia, Ana C. L. and Gardiner, Anastasia and Garfield, David A. and Garvin, Barry E. and Gibson, Greg and Gilbert, Don and Gnerre, Sante and Godfrey, Jennifer and Good, Robert and Gotea, Valer and Gravely, Brenton and Greenberg, Anthony J. and Griffiths-Jones, Sam and Gross, Samuel and Guigo, Roderic and Gustafson, Erik A. and Haerty, Wilfried and Hahn, Matthew W. and Halligan, Daniel L. and Halpern, Aaron L. and Halter, Gillian M. and Han, Mira V. and Heger, Andreas and Hillier, LaDeana and Hinrichs, Angie S. and Holmes, Ian and Hoskins, Roger A. and Hubisz, Melissa J. and Hultmark, Dan and Huntley, Melanie A. and Jaffe, David B. and Jagadeeshan, Santosh and Jeck, William R. and Johnson, Justin and Jones, Corbin D. and Jordan, William C. and Karpen, Gary H. and Kataoka, Eiko and Keightley, Peter D. and Kheradpour, Pouya and Kirkness, Ewen F. and Koerich, Leonardo B. and Kristiansen, Karsten and Kudrna, Dave and Kulathinal, Rob J. and Kumar, Sudhir and Kwok, Roberta and Lander, Eric and Langley, Charles H. and Lapoint, Richard and Lazzaro, Brian P. and Lee, So-Jeong and Levesque, Lisa and Li, Ruiqiang and Lin, Chiao-Feng and Lin, Michael F. and Lindblad-Toh, Kerstin and Llopart, Ana and Long, Manyuan and Low, Lloyd and Lozovsky, Elena and Lu, Jian and Luo, Meizhong and Machado, Carlos A. and Makalowski, Wojciech and Marzo, Mar and Matsuda, Muneo and Matzkin, Luciano and McAllister, Bryant and McBride, Carolyn S. and McKernan, Brendan and McKernan, Kevin and Mendez-Lago, Maria and Minx, Patrick and Mollenhauer, Michael U. and Montooth, Kristi and Stephen M. Mount and Mu, Xu and Myers, Eugene and Negre, Barbara and Newfeld, Stuart and Nielsen, Rasmus and Noor, Mohamed A. F. and O{\textquoteright}Grady, Patrick and Pachter, Lior and Papaceit, Montserrat and Parisi, Matthew J. and Parisi, Michael and Parts, Leopold and Pedersen, Jakob S. and Pesole, Graziano and Phillippy, Adam M. and Ponting, Chris P. and M. Pop and Porcelli, Damiano and Powell, Jeffrey R. and Prohaska, Sonja and Pruitt, Kim and Puig, Marta and Quesneville, Hadi and Ram, Kristipati Ravi and Rand, David and Rasmussen, Matthew D. and Reed, Laura K. and Reenan, Robert and Reily, Amy and Remington, Karin A. and Rieger, Tania T. and Ritchie, Michael G. and Robin, Charles and Rogers, Yu-Hui and Rohde, Claudia and Rozas, Julio and Rubenfield, Marc J. and Ruiz, Alfredo and Russo, Susan and Salzberg, Steven L. and Sanchez-Gracia, Alejandro and Saranga, David J. and Sato, Hajime and Schaeffer, Stephen W. and Schatz, Michael C. and Schlenke, Todd and Schwartz, Russell and Segarra, Carmen and Singh, Rama S. and Sirot, Laura and Sirota, Marina and Sisneros, Nicholas B. and Smith, Chris D. and Smith, Temple F. and Spieth, John and Stage, Deborah E. and Stark, Alexander and Stephan, Wolfgang and Strausberg, Robert L. and Strempel, Sebastian and Sturgill, David and Sutton, Granger and Sutton, Granger G. and Tao, Wei and Teichmann, Sarah and Tobari, Yoshiko N. and Tomimura, Yoshihiko and Tsolas, Jason M. and Valente, Vera L. S. and Venter, Eli and Venter, J. Craig and Vicario, Saverio and Vieira, Filipe G. and Vilella, Albert J. and Villasante, Alfredo and Walenz, Brian and Wang, Jun and Wasserman, Marvin and Watts, Thomas and Wilson, Derek and Wilson, Richard K. and Wing, Rod A. and Wolfner, Mariana F. and Wong, Alex and Wong, Gane Ka-Shu and Wu, Chung- I. and Wu, Gabriel and Yamamoto, Daisuke and Yang, Hsiao-Pei and Yang, Shiaw-Pyng and Yorke, James A. and Yoshida, Kiyohito and Zdobnov, Evgeny and Zhang, Peili and Zhang, Yu and Zimin, Aleksey V. and Baldwin, Jennifer and Abdouelleil, Amr and Abdulkadir, Jamal and Abebe, Adal and Abera, Brikti and Abreu, Justin and Acer, St Christophe and Aftuck, Lynne and Alexander, Allen and An, Peter and Anderson, Erica and Anderson, Scott and Arachi, Harindra and Azer, Marc and Bachantsang, Pasang and Barry, Andrew and Bayul, Tashi and Berlin, Aaron and Bessette, Daniel and Bloom, Toby and Blye, Jason and Boguslavskiy, Leonid and Bonnet, Claude and Boukhgalter, Boris and Bourzgui, Imane and Brown, Adam and Cahill, Patrick and Channer, Sheridon and Cheshatsang, Yama and Chuda, Lisa and Citroen, Mieke and Collymore, Alville and Cooke, Patrick and Costello, Maura and D{\textquoteright}Aco, Katie and Daza, Riza and Haan, Georgius De and DeGray, Stuart and DeMaso, Christina and Dhargay, Norbu and Dooley, Kimberly and Dooley, Erin and Doricent, Missole and Dorje, Passang and Dorjee, Kunsang and Dupes, Alan and Elong, Richard and Falk, Jill and Farina, Abderrahim and Faro, Susan and Ferguson, Diallo and Fisher, Sheila and Foley, Chelsea D. and Franke, Alicia and Friedrich, Dennis and Gadbois, Loryn and Gearin, Gary and Gearin, Christina R. and Giannoukos, Georgia and Goode, Tina and Graham, Joseph and Grandbois, Edward and Grewal, Sharleen and Gyaltsen, Kunsang and Hafez, Nabil and Hagos, Birhane and Hall, Jennifer and Henson, Charlotte and Hollinger, Andrew and Honan, Tracey and Huard, Monika D. and Hughes, Leanne and Hurhula, Brian and Husby, M. Erii and Kamat, Asha and Kanga, Ben and Kashin, Seva and Khazanovich, Dmitry and Kisner, Peter and Lance, Krista and Lara, Marcia and Lee, William and Lennon, Niall and Letendre, Frances and LeVine, Rosie and Lipovsky, Alex and Liu, Xiaohong and Liu, Jinlei and Liu, Shangtao and Lokyitsang, Tashi and Lokyitsang, Yeshi and Lubonja, Rakela and Lui, Annie and MacDonald, Pen and Magnisalis, Vasilia and Maru, Kebede and Matthews, Charles and McCusker, William and McDonough, Susan and Mehta, Teena and Meldrim, James and Meneus, Louis and Mihai, Oana and Mihalev, Atanas and Mihova, Tanya and Mittelman, Rachel and Mlenga, Valentine and Montmayeur, Anna and Mulrain, Leonidas and Navidi, Adam and Naylor, Jerome and Negash, Tamrat and Nguyen, Thu and Nguyen, Nga and Nicol, Robert and Norbu, Choe and Norbu, Nyima and Novod, Nathaniel and O{\textquoteright}Neill, Barry and Osman, Sahal and Markiewicz, Eva and Oyono, Otero L. and Patti, Christopher and Phunkhang, Pema and Pierre, Fritz and Priest, Margaret and Raghuraman, Sujaa and Rege, Filip and Reyes, Rebecca and Rise, Cecil and Rogov, Peter and Ross, Keenan and Ryan, Elizabeth and Settipalli, Sampath and Shea, Terry and Sherpa, Ngawang and Shi, Lu and Shih, Diana and Sparrow, Todd and Spaulding, Jessica and Stalker, John and Stange-Thomann, Nicole and Stavropoulos, Sharon and Stone, Catherine and Strader, Christopher and Tesfaye, Senait and Thomson, Talene and Thoulutsang, Yama and Thoulutsang, Dawa and Topham, Kerri and Topping, Ira and Tsamla, Tsamla and Vassiliev, Helen and Vo, Andy and Wangchuk, Tsering and Wangdi, Tsering and Weiand, Michael and Wilkinson, Jane and Wilson, Adam and Yadav, Shailendra and Young, Geneva and Yu, Qing and Zembek, Lisa and Zhong, Danni and Zimmer, Andrew and Zwirko, Zac and Jaffe, David B. and Alvarez, Pablo and Brockman, Will and Butler, Jonathan and Chin, CheeWhye and Gnerre, Sante and Grabherr, Manfred and Kleber, Michael and Mauceli, Evan and MacCallum, Iain} } @article {49677, title = {Evolution of genes and genomes on the Drosophila phylogeny.}, journal = {Nature}, volume = {450}, year = {2007}, month = {2007 Nov 8}, pages = {203-18}, abstract = {

Comparative analysis of multiple genomes in a phylogenetic framework dramatically improves the precision and sensitivity of evolutionary inference, producing more robust results than single-genome analyses can provide. The genomes of 12 Drosophila species, ten of which are presented here for the first time (sechellia, simulans, yakuba, erecta, ananassae, persimilis, willistoni, mojavensis, virilis and grimshawi), illustrate how rates and patterns of sequence divergence across taxa can illuminate evolutionary processes on a genomic scale. These genome sequences augment the formidable genetic tools that have made Drosophila melanogaster a pre-eminent model for animal genetics, and will further catalyse fundamental research on mechanisms of development, cell biology, genetics, disease, neurobiology, behaviour, physiology and evolution. Despite remarkable similarities among these Drosophila species, we identified many putatively non-neutral changes in protein-coding genes, non-coding RNA genes, and cis-regulatory regions. These may prove to underlie differences in the ecology and behaviour of these diverse species.

}, keywords = {Animals, Codon, DNA Transposable Elements, Drosophila, Drosophila Proteins, Evolution, Molecular, Gene Order, Genes, Insect, Genome, Insect, Genome, Mitochondrial, Genomics, Immunity, Multigene Family, Phylogeny, Reproduction, RNA, Untranslated, sequence alignment, Sequence Analysis, DNA, Synteny}, issn = {1476-4687}, doi = {10.1038/nature06341}, author = {Clark, Andrew G and Eisen, Michael B and Smith, Douglas R and Bergman, Casey M and Oliver, Brian and Markow, Therese A and Kaufman, Thomas C and Kellis, Manolis and Gelbart, William and Iyer, Venky N and Pollard, Daniel A and Sackton, Timothy B and Larracuente, Amanda M and Singh, Nadia D and Abad, Jose P and Abt, Dawn N and Adryan, Boris and Aguade, Montserrat and Akashi, Hiroshi and Anderson, Wyatt W and Aquadro, Charles F and Ardell, David H and Arguello, Roman and Artieri, Carlo G and Barbash, Daniel A and Barker, Daniel and Barsanti, Paolo and Batterham, Phil and Batzoglou, Serafim and Begun, Dave and Bhutkar, Arjun and Blanco, Enrico and Bosak, Stephanie A and Bradley, Robert K and Brand, Adrianne D and Brent, Michael R and Brooks, Angela N and Brown, Randall H and Butlin, Roger K and Caggese, Corrado and Calvi, Brian R and Bernardo de Carvalho, A and Caspi, Anat and Castrezana, Sergio and Celniker, Susan E and Chang, Jean L and Chapple, Charles and Chatterji, Sourav and Chinwalla, Asif and Civetta, Alberto and Clifton, Sandra W and Comeron, Josep M and Costello, James C and Coyne, Jerry A and Daub, Jennifer and David, Robert G and Delcher, Arthur L and Delehaunty, Kim and Do, Chuong B and Ebling, Heather and Edwards, Kevin and Eickbush, Thomas and Evans, Jay D and Filipski, Alan and Findeiss, Sven and Freyhult, Eva and Fulton, Lucinda and Fulton, Robert and Garcia, Ana C L and Gardiner, Anastasia and Garfield, David A and Garvin, Barry E and Gibson, Greg and Gilbert, Don and Gnerre, Sante and Godfrey, Jennifer and Good, Robert and Gotea, Valer and Gravely, Brenton and Greenberg, Anthony J and Griffiths-Jones, Sam and Gross, Samuel and Guigo, Roderic and Gustafson, Erik A and Haerty, Wilfried and Hahn, Matthew W and Halligan, Daniel L and Halpern, Aaron L and Halter, Gillian M and Han, Mira V and Heger, Andreas and Hillier, LaDeana and Hinrichs, Angie S and Holmes, Ian and Hoskins, Roger A and Hubisz, Melissa J and Hultmark, Dan and Huntley, Melanie A and Jaffe, David B and Jagadeeshan, Santosh and Jeck, William R and Johnson, Justin and Jones, Corbin D and Jordan, William C and Karpen, Gary H and Kataoka, Eiko and Keightley, Peter D and Kheradpour, Pouya and Kirkness, Ewen F and Koerich, Leonardo B and Kristiansen, Karsten and Kudrna, Dave and Kulathinal, Rob J and Kumar, Sudhir and Kwok, Roberta and Lander, Eric and Langley, Charles H and Lapoint, Richard and Lazzaro, Brian P and Lee, So-Jeong and Levesque, Lisa and Li, Ruiqiang and Lin, Chiao-Feng and Lin, Michael F and Lindblad-Toh, Kerstin and Llopart, Ana and Long, Manyuan and Low, Lloyd and Lozovsky, Elena and Lu, Jian and Luo, Meizhong and Machado, Carlos A and Makalowski, Wojciech and Marzo, Mar and Matsuda, Muneo and Matzkin, Luciano and McAllister, Bryant and McBride, Carolyn S and McKernan, Brendan and McKernan, Kevin and Mendez-Lago, Maria and Minx, Patrick and Mollenhauer, Michael U and Montooth, Kristi and Mount, Stephen M and Mu, Xu and Myers, Eugene and Negre, Barbara and Newfeld, Stuart and Nielsen, Rasmus and Noor, Mohamed A F and O{\textquoteright}Grady, Patrick and Pachter, Lior and Papaceit, Montserrat and Parisi, Matthew J and Parisi, Michael and Parts, Leopold and Pedersen, Jakob S and Pesole, Graziano and Phillippy, Adam M and Ponting, Chris P and Pop, Mihai and Porcelli, Damiano and Powell, Jeffrey R and Prohaska, Sonja and Pruitt, Kim and Puig, Marta and Quesneville, Hadi and Ram, Kristipati Ravi and Rand, David and Rasmussen, Matthew D and Reed, Laura K and Reenan, Robert and Reily, Amy and Remington, Karin A and Rieger, Tania T and Ritchie, Michael G and Robin, Charles and Rogers, Yu-Hui and Rohde, Claudia and Rozas, Julio and Rubenfield, Marc J and Ruiz, Alfredo and Russo, Susan and Salzberg, Steven L and Sanchez-Gracia, Alejandro and Saranga, David J and Sato, Hajime and Schaeffer, Stephen W and Schatz, Michael C and Schlenke, Todd and Schwartz, Russell and Segarra, Carmen and Singh, Rama S and Sirot, Laura and Sirota, Marina and Sisneros, Nicholas B and Smith, Chris D and Smith, Temple F and Spieth, John and Stage, Deborah E and Stark, Alexander and Stephan, Wolfgang and Strausberg, Robert L and Strempel, Sebastian and Sturgill, David and Sutton, Granger and Sutton, Granger G and Tao, Wei and Teichmann, Sarah and Tobari, Yoshiko N and Tomimura, Yoshihiko and Tsolas, Jason M and Valente, Vera L S and Venter, Eli and Venter, J Craig and Vicario, Saverio and Vieira, Filipe G and Vilella, Albert J and Villasante, Alfredo and Walenz, Brian and Wang, Jun and Wasserman, Marvin and Watts, Thomas and Wilson, Derek and Wilson, Richard K and Wing, Rod A and Wolfner, Mariana F and Wong, Alex and Wong, Gane Ka-Shu and Wu, Chung-I and Wu, Gabriel and Yamamoto, Daisuke and Yang, Hsiao-Pei and Yang, Shiaw-Pyng and Yorke, James A and Yoshida, Kiyohito and Zdobnov, Evgeny and Zhang, Peili and Zhang, Yu and Zimin, Aleksey V and Baldwin, Jennifer and Abdouelleil, Amr and Abdulkadir, Jamal and Abebe, Adal and Abera, Brikti and Abreu, Justin and Acer, St Christophe and Aftuck, Lynne and Alexander, Allen and An, Peter and Anderson, Erica and Anderson, Scott and Arachi, Harindra and Azer, Marc and Bachantsang, Pasang and Barry, Andrew and Bayul, Tashi and Berlin, Aaron and Bessette, Daniel and Bloom, Toby and Blye, Jason and Boguslavskiy, Leonid and Bonnet, Claude and Boukhgalter, Boris and Bourzgui, Imane and Brown, Adam and Cahill, Patrick and Channer, Sheridon and Cheshatsang, Yama and Chuda, Lisa and Citroen, Mieke and Collymore, Alville and Cooke, Patrick and Costello, Maura and D{\textquoteright}Aco, Katie and Daza, Riza and De Haan, Georgius and DeGray, Stuart and DeMaso, Christina and Dhargay, Norbu and Dooley, Kimberly and Dooley, Erin and Doricent, Missole and Dorje, Passang and Dorjee, Kunsang and Dupes, Alan and Elong, Richard and Falk, Jill and Farina, Abderrahim and Faro, Susan and Ferguson, Diallo and Fisher, Sheila and Foley, Chelsea D and Franke, Alicia and Friedrich, Dennis and Gadbois, Loryn and Gearin, Gary and Gearin, Christina R and Giannoukos, Georgia and Goode, Tina and Graham, Joseph and Grandbois, Edward and Grewal, Sharleen and Gyaltsen, Kunsang and Hafez, Nabil and Hagos, Birhane and Hall, Jennifer and Henson, Charlotte and Hollinger, Andrew and Honan, Tracey and Huard, Monika D and Hughes, Leanne and Hurhula, Brian and Husby, M Erii and Kamat, Asha and Kanga, Ben and Kashin, Seva and Khazanovich, Dmitry and Kisner, Peter and Lance, Krista and Lara, Marcia and Lee, William and Lennon, Niall and Letendre, Frances and LeVine, Rosie and Lipovsky, Alex and Liu, Xiaohong and Liu, Jinlei and Liu, Shangtao and Lokyitsang, Tashi and Lokyitsang, Yeshi and Lubonja, Rakela and Lui, Annie and MacDonald, Pen and Magnisalis, Vasilia and Maru, Kebede and Matthews, Charles and McCusker, William and McDonough, Susan and Mehta, Teena and Meldrim, James and Meneus, Louis and Mihai, Oana and Mihalev, Atanas and Mihova, Tanya and Mittelman, Rachel and Mlenga, Valentine and Montmayeur, Anna and Mulrain, Leonidas and Navidi, Adam and Naylor, Jerome and Negash, Tamrat and Nguyen, Thu and Nguyen, Nga and Nicol, Robert and Norbu, Choe and Norbu, Nyima and Novod, Nathaniel and O{\textquoteright}Neill, Barry and Osman, Sahal and Markiewicz, Eva and Oyono, Otero L and Patti, Christopher and Phunkhang, Pema and Pierre, Fritz and Priest, Margaret and Raghuraman, Sujaa and Rege, Filip and Reyes, Rebecca and Rise, Cecil and Rogov, Peter and Ross, Keenan and Ryan, Elizabeth and Settipalli, Sampath and Shea, Terry and Sherpa, Ngawang and Shi, Lu and Shih, Diana and Sparrow, Todd and Spaulding, Jessica and Stalker, John and Stange-Thomann, Nicole and Stavropoulos, Sharon and Stone, Catherine and Strader, Christopher and Tesfaye, Senait and Thomson, Talene and Thoulutsang, Yama and Thoulutsang, Dawa and Topham, Kerri and Topping, Ira and Tsamla, Tsamla and Vassiliev, Helen and Vo, Andy and Wangchuk, Tsering and Wangdi, Tsering and Weiand, Michael and Wilkinson, Jane and Wilson, Adam and Yadav, Shailendra and Young, Geneva and Yu, Qing and Zembek, Lisa and Zhong, Danni and Zimmer, Andrew and Zwirko, Zac and Jaffe, David B and Alvarez, Pablo and Brockman, Will and Butler, Jonathan and Chin, CheeWhye and Gnerre, Sante and Grabherr, Manfred and Kleber, Michael and Mauceli, Evan and MacCallum, Iain} } @article {49782, title = {Genome sequence and identification of candidate vaccine antigens from the animal pathogen Dichelobacter nodosus.}, journal = {Nat Biotechnol}, volume = {25}, year = {2007}, month = {2007 May}, pages = {569-75}, abstract = {

Dichelobacter nodosus causes ovine footrot, a disease that leads to severe economic losses in the wool and meat industries. We sequenced its 1.4-Mb genome, the smallest known genome of an anaerobe. It differs markedly from small genomes of intracellular bacteria, retaining greater biosynthetic capabilities and lacking any evidence of extensive ongoing genome reduction. Comparative genomic microarray studies and bioinformatic analysis suggested that, despite its small size, almost 20\% of the genome is derived from lateral gene transfer. Most of these regions seem to be associated with virulence. Metabolic reconstruction indicated unsuspected capabilities, including carbohydrate utilization, electron transfer and several aerobic pathways. Global transcriptional profiling and bioinformatic analysis enabled the prediction of virulence factors and cell surface proteins. Screening of these proteins against ovine antisera identified eight immunogenic proteins that are candidate antigens for a cross-protective vaccine.

}, keywords = {Animals, Antigens, Chromosome mapping, Dichelobacter nodosus, Foot Rot, Genome, Bacterial, Sequence Analysis, DNA}, issn = {1087-0156}, doi = {10.1038/nbt1302}, author = {Myers, Garry S A and Parker, Dane and Al-Hasani, Keith and Kennan, Ruth M and Seemann, Torsten and Ren, Qinghu and Badger, Jonathan H and Selengut, Jeremy D and DeBoy, Robert T and Tettelin, Herv{\'e} and Boyce, John D and McCarl, Victoria P and Han, Xiaoyan and Nelson, William C and Madupu, Ramana and Mohamoud, Yasmin and Holley, Tara and Fedorova, Nadia and Khouri, Hoda and Bottomley, Steven P and Whittington, Richard J and Adler, Ben and Songer, J Glenn and Rood, Julian I and Paulsen, Ian T} } @article {38296, title = {Genome sequence and identification of candidate vaccine antigens from the animal pathogen Dichelobacter nodosus}, journal = {Nature biotechnologyNature biotechnology}, volume = {25}, year = {2007}, note = {http://www.ncbi.nlm.nih.gov/pubmed/17468768?dopt=Abstract}, type = {10.1038/nbt1302}, abstract = {Dichelobacter nodosus causes ovine footrot, a disease that leads to severe economic losses in the wool and meat industries. We sequenced its 1.4-Mb genome, the smallest known genome of an anaerobe. It differs markedly from small genomes of intracellular bacteria, retaining greater biosynthetic capabilities and lacking any evidence of extensive ongoing genome reduction. Comparative genomic microarray studies and bioinformatic analysis suggested that, despite its small size, almost 20\% of the genome is derived from lateral gene transfer. Most of these regions seem to be associated with virulence. Metabolic reconstruction indicated unsuspected capabilities, including carbohydrate utilization, electron transfer and several aerobic pathways. Global transcriptional profiling and bioinformatic analysis enabled the prediction of virulence factors and cell surface proteins. Screening of these proteins against ovine antisera identified eight immunogenic proteins that are candidate antigens for a cross-protective vaccine.}, keywords = {Animals, Antigens, Chromosome mapping, Dichelobacter nodosus, Foot Rot, Genome, Bacterial, Sequence Analysis, DNA}, author = {Myers, Garry S. A. and Parker, Dane and Al-Hasani, Keith and Kennan, Ruth M. and Seemann, Torsten and Ren, Qinghu and Badger, Jonathan H. and J. Selengut and DeBoy, Robert T. and Tettelin, Herv{\'e} and Boyce, John D. and McCarl, Victoria P. and Han, Xiaoyan and Nelson, William C. and Madupu, Ramana and Mohamoud, Yasmin and Holley, Tara and Fedorova, Nadia and Khouri, Hoda and Bottomley, Steven P. and Whittington, Richard J. and Adler, Ben and Songer, J. Glenn and Rood, Julian I. and Paulsen, Ian T.} } @article {38323, title = {Grid Services Base Library: A high-level, procedural application programming interface for writing Globus-based Grid services}, journal = {Future Generation Comp SystFuture Generation Comp Syst}, volume = {23}, year = {2007}, abstract = {The Grid Services Base Library (GSBL) is a procedural application programming interface (API) that abstracts many of the high-level functions performed by Globus Grid services, thus dramatically lowering the barriers to writing Grid services. The library has been extensively tested and used for computational biology research in a Globus Toolkit-based Grid system, in which no fewer than twenty Grid services written with this API are deployed.}, author = {Adam L. Bazinet and Myers, D. S. and Fuetsch, J. and Michael P. Cummings} } @article {38377, title = {Microarray analysis of gene expression induced by sexual contact in Schistosoma mansoni}, journal = {BMC GenomicsBMC Genomics}, volume = {8}, year = {2007}, type = {10.1186/1471-2164-8-181}, abstract = {BACKGROUND:The parasitic trematode Schistosoma mansoni is one of the major causative agents of Schistosomiasis, a disease that affects approximately 200 million people, mostly in developing countries. Since much of the pathology is associated with eggs laid by the female worm, understanding the mechanisms involved in oogenesis and sexual maturation is an important step towards the discovery of new targets for effective drug therapy. It is known that the adult female worm only develops fully in the presence of a male worm and that the rates of oviposition and maturation of eggs are significantly increased by mating. In order to study gene transcripts associated with sexual maturation and oviposition, we compared the gene expression profiles of sexually mature and immature parasites using DNA microarrays.RESULTS:For each experiment, three amplified RNA microarray hybridizations and their dye swaps were analyzed. Our results show that 265 transcripts are differentially expressed in adult females and 53 in adult males when mature and immature worms are compared. Of the genes differentially expressed, 55\% are expressed at higher levels in paired females while the remaining 45\% are more expressed in unpaired ones and 56.6\% are expressed at higher levels in paired male worms while the remaining 43.4\% are more expressed in immature parasites. Real-time RT-PCR analysis validated the microarray results. Several new maturation associated transcripts were identified. Genes that were up-regulated in single-sex females were mostly related to energy generation (i.e. carbohydrate and protein metabolism, generation of precursor metabolites and energy, cellular catabolism, and organelle organization and biogenesis) while genes that were down-regulated related to RNA metabolism, reactive oxygen species metabolism, electron transport, organelle organization and biogenesis and protein biosynthesis.CONCLUSION:Our results confirm previous observations related to gene expression induced by sexual maturation in female schistosome worms. They also increase the list of S. mansoni maturation associated transcripts considerably, therefore opening new and exciting avenues for the study of the conjugal biology and development of new drugs against schistosomes.}, isbn = {1471-2164}, author = {Waisberg, Michael and Lobo, Francisco and Cerqueira, Gustavo and Passos, Liana and Carvalho, Omar and Franco, Gloria and Najib M. El-Sayed} } @article {49783, title = {New developments in the InterPro database.}, journal = {Nucleic Acids Res}, volume = {35}, year = {2007}, month = {2007 Jan}, pages = {D224-8}, abstract = {

InterPro is an integrated resource for protein families, domains and functional sites, which integrates the following protein signature databases: PROSITE, PRINTS, ProDom, Pfam, SMART, TIGRFAMs, PIRSF, SUPERFAMILY, Gene3D and PANTHER. The latter two new member databases have been integrated since the last publication in this journal. There have been several new developments in InterPro, including an additional reading field, new database links, extensions to the web interface and additional match XML files. InterPro has always provided matches to UniProtKB proteins on the website and in the match XML file on the FTP site. Additional matches to proteins in UniParc (UniProt archive) are now available for download in the new match XML files only. The latest InterPro release (13.0) contains more than 13 000 entries, covering over 78\% of all proteins in UniProtKB. The database is available for text- and sequence-based searches via a webserver (http://www.ebi.ac.uk/interpro), and for download by anonymous FTP (ftp://ftp.ebi.ac.uk/pub/databases/interpro). The InterProScan search tool is now also available via a web service at http://www.ebi.ac.uk/Tools/webservices/WSInterProScan.html.

}, keywords = {Databases, Protein, Internet, Protein Structure, Tertiary, Proteins, Sequence Analysis, Protein, Systems Integration, User-Computer Interface}, issn = {1362-4962}, doi = {10.1093/nar/gkl841}, author = {Mulder, Nicola J and Apweiler, Rolf and Attwood, Teresa K and Bairoch, Amos and Bateman, Alex and Binns, David and Bork, Peer and Buillard, Virginie and Cerutti, Lorenzo and Copley, Richard and Courcelle, Emmanuel and Das, Ujjwal and Daugherty, Louise and Dibley, Mark and Finn, Robert and Fleischmann, Wolfgang and Gough, Julian and Haft, Daniel and Hulo, Nicolas and Hunter, Sarah and Kahn, Daniel and Kanapin, Alexander and Kejariwal, Anish and Labarga, Alberto and Langendijk-Genevaux, Petra S and Lonsdale, David and Lopez, Rodrigo and Letunic, Ivica and Madera, Martin and Maslen, John and McAnulla, Craig and McDowall, Jennifer and Mistry, Jaina and Mitchell, Alex and Nikolskaya, Anastasia N and Orchard, Sandra and Orengo, Christine and Petryszak, Robert and Selengut, Jeremy D and Sigrist, Christian J A and Thomas, Paul D and Valentin, Franck and Wilson, Derek and Wu, Cathy H and Yeats, Corin} } @article {38161, title = {Comparative genomics of emerging human ehrlichiosis agents}, journal = {PLoS geneticsPLoS genetics}, volume = {2}, year = {2006}, note = {http://www.ncbi.nlm.nih.gov/pubmed/16482227?dopt=Abstract}, type = {10.1371/journal.pgen.0020021}, abstract = {Anaplasma (formerly Ehrlichia) phagocytophilum, Ehrlichia chaffeensis, and Neorickettsia (formerly Ehrlichia) sennetsu are intracellular vector-borne pathogens that cause human ehrlichiosis, an emerging infectious disease. We present the complete genome sequences of these organisms along with comparisons to other organisms in the Rickettsiales order. Ehrlichia spp. and Anaplasma spp. display a unique large expansion of immunodominant outer membrane proteins facilitating antigenic variation. All Rickettsiales have a diminished ability to synthesize amino acids compared to their closest free-living relatives. Unlike members of the Rickettsiaceae family, these pathogenic Anaplasmataceae are capable of making all major vitamins, cofactors, and nucleotides, which could confer a beneficial role in the invertebrate vector or the vertebrate host. Further analysis identified proteins potentially involved in vacuole confinement of the Anaplasmataceae, a life cycle involving a hematophagous vector, vertebrate pathogenesis, human pathogenesis, and lack of transovarial transmission. These discoveries provide significant insights into the biology of these obligate intracellular pathogens.}, keywords = {Animals, Biotin, DNA Repair, Ehrlichia, Ehrlichiosis, Genome, Genomics, HUMANS, Models, Biological, Phylogeny, Rickettsia, Ticks}, author = {Dunning Hotopp, Julie C. and Lin, Mingqun and Madupu, Ramana and Crabtree, Jonathan and Angiuoli, Samuel V. and Eisen, Jonathan A. and Eisen, Jonathan and Seshadri, Rekha and Ren, Qinghu and Wu, Martin and Utterback, Teresa R. and Smith, Shannon and Lewis, Matthew and Khouri, Hoda and Zhang, Chunbin and Niu, Hua and Lin, Quan and Ohashi, Norio and Zhi, Ning and Nelson, William and Brinkac, Lauren M. and Dodson, Robert J. and Rosovitz, M. J. and Sundaram, Jaideep and Daugherty, Sean C. and Davidsen, Tanja and Durkin, Anthony S. and Gwinn, Michelle and Haft, Daniel H. and J. Selengut and Sullivan, Steven A. and Zafar, Nikhat and Zhou, Liwei and Benahmed, Faiza and Forberger, Heather and Halpin, Rebecca and Mulligan, Stephanie and Robinson, Jeffrey and White, Owen and Rikihisa, Yasuko and Tettelin, Herv{\'e}} } @article {49751, title = {How A.I. and multi-robot systems research will accelerate our understanding of social animal behavior}, volume = {94}, year = {2006}, pages = {1445-1463}, author = {Tucker Balch and Frank Dellaert and Adam Feldman and Andrew Guillory and Charles Isbell and Zia Khan and Andrew Stein and Hank Wilde} } @article {49561, title = {How Multirobot Systems Research will Accelerate our Understanding of Social Animal Behavior}, volume = {94}, year = {2006}, month = {Jan-07-2006}, pages = {1445 - 1463}, issn = {0018-9219}, doi = {10.1109/JPROC.2006.876969}, url = {http://ieeexplore.ieee.org/lpdocs/epic03/wrapper.htm?arnumber=1677955}, author = {Balch, T. and Dellaert, F. and Feldman, A. and Guillory, A. and Isbell, C.L. and Khan, Z. and Pratt, S.C. and Stein, A.N. and Wilde, H.} } @article {38371, title = {Metagenomic Analysis of the Human Distal Gut Microbiome}, journal = {ScienceScienceScienceScience}, volume = {312}, year = {2006}, type = {10.1126/science.1124234}, abstract = {The human intestinal microbiota is composed of 1013 to 1014 microorganisms whose collective genome ({\textquotedblleft}microbiome{\textquotedblright}) contains at least 100 times as many genes as our own genome. We analyzed \~{}78 million base pairs of unique DNA sequence and 2062 polymerase chain reaction{\textendash}amplified 16S ribosomal DNA sequences obtained from the fecal DNAs of two healthy adults. Using metabolic function analyses of identified genes, we compared our human genome with the average content of previously sequenced microbial genomes. Our microbiome has significantly enriched metabolism of glycans, amino acids, and xenobiotics; methanogenesis; and 2-methyl-d-erythritol 4-phosphate pathway{\textendash}mediated biosynthesis of vitamins and isoprenoids. Thus, humans are superorganisms whose metabolism represents an amalgamation of microbial and human attributes.}, isbn = {0036-8075, 1095-9203}, author = {Gill, Steven R. and M. Pop and DeBoy, Robert T. and Eckburg, Paul B. and Turnbaugh, Peter J. and Samuel, Buck S. and Gordon, Jeffrey I. and Relman, David A. and Fraser-Liggett, Claire M. and Nelson, Karen E.} } @article {38387, title = {Molecular Characterization of Serine-, Alanine-, and Proline-Rich Proteins of Trypanosoma cruzi and Their Possible Role in Host Cell Infection}, journal = {Infect. Immun.Infect. Immun.}, volume = {74}, year = {2006}, type = {

10.1128/IAI.74.3.1537-1546.2006

}, abstract = {We previously reported the isolation of a novel protein gene family, termed SAP (serine-, alanine-, and proline-rich protein), from Trypanosoma cruzi. Aided by the availability of the completed genome sequence of T. cruzi, we have now identified 39 full-length sequences of SAP, six pseudogenes and four partial genes. SAPs share a central domain of about 55 amino acids and can be divided into four groups based on their amino (N)- and carboxy (C)-terminal sequences. Some SAPs have conserved N- and C-terminal domains encoding a signal peptide and a glycosylphosphatidylinositol anchor addition site, respectively. Analysis of the expression of SAPs in metacyclic trypomastigotes by two-dimensional electrophoresis and immunoblotting revealed that they are likely to be posttranslationally modified in vivo. We have also demonstrated that some SAPs are shed into the extracellular medium. The recombinant SAP exhibited an adhesive capacity toward mammalian cells, where binding was dose dependent and saturable, indicating a possible ligand-receptor interaction. SAP triggered the host cell Ca2+ response required for parasite internalization. A cell invasion assay performed in the presence of SAP showed inhibition of internalization of the metacyclic forms of the CL strain. Taken together, these results show that SAP is involved in the invasion of mammalian cells by metacyclic trypomastigotes, and they confirm the hypothesis that infective trypomastigotes exploit an arsenal of surface glycoproteins and shed proteins to induce signaling events required for their internalization.}, author = {Baida, Renata C. P. and Santos, Marcia R. M. and Carmo, Mirian S. and Yoshida, Nobuko and Ferreira, Danielle and Ferreira, Alice Teixeira and El Sayed, Najib M. and Andersson, Bj{\"o}rn and da Silveira, Jose Franco} } @article {38227, title = {eGenomics: Cataloguing our Complete Genome Collection}, journal = {Comparative and functional genomicsComparative and functional genomics}, volume = {6}, year = {2005}, note = {http://www.ncbi.nlm.nih.gov/pubmed/18629208?dopt=Abstract}, type = {10.1002/cfg.494}, author = {Field, Dawn and Garrity, George and Morrison, Norman and J. Selengut and Sterk, Peter and Tatusova, Tatiana and Thomson, Nick} } @article {38287, title = {Genome analysis of multiple pathogenic isolates of Streptococcus agalactiae: implications for the microbial "pan-genome"}, journal = {Proceedings of the National Academy of Sciences of the United States of AmericaProceedings of the National Academy of Sciences of the United States of America}, volume = {102}, year = {2005}, note = {http://www.ncbi.nlm.nih.gov/pubmed/16172379?dopt=Abstract}, type = {10.1073/pnas.0506758102}, abstract = {The development of efficient and inexpensive genome sequencing methods has revolutionized the study of human bacterial pathogens and improved vaccine design. Unfortunately, the sequence of a single genome does not reflect how genetic variability drives pathogenesis within a bacterial species and also limits genome-wide screens for vaccine candidates or for antimicrobial targets. We have generated the genomic sequence of six strains representing the five major disease-causing serotypes of Streptococcus agalactiae, the main cause of neonatal infection in humans. Analysis of these genomes and those available in databases showed that the S. agalactiae species can be described by a pan-genome consisting of a core genome shared by all isolates, accounting for approximately 80\% of any single genome, plus a dispensable genome consisting of partially shared and strain-specific genes. Mathematical extrapolation of the data suggests that the gene reservoir available for inclusion in the S. agalactiae pan-genome is vast and that unique genes will continue to be identified even after sequencing hundreds of genomes.}, keywords = {Amino Acid Sequence, Bacterial Capsules, Base Sequence, Gene expression, Genes, Bacterial, Genetic Variation, Genome, Bacterial, Molecular Sequence Data, Phylogeny, sequence alignment, Sequence Analysis, DNA, Streptococcus agalactiae, virulence}, author = {Tettelin, Herv{\'e} and Masignani, Vega and Cieslewicz, Michael J. and Donati, Claudio and Medini, Duccio and Ward, Naomi L. and Angiuoli, Samuel V. and Crabtree, Jonathan and Jones, Amanda L. and Durkin, A. Scott and DeBoy, Robert T. and Davidsen, Tanja M. and Mora, Marirosa and Scarselli, Maria and Margarit y Ros, Immaculada and Peterson, Jeremy D. and Hauser, Christopher R. and Sundaram, Jaideep P. and Nelson, William C. and Madupu, Ramana and Brinkac, Lauren M. and Dodson, Robert J. and Rosovitz, Mary J. and Sullivan, Steven A. and Daugherty, Sean C. and Haft, Daniel H. and J. Selengut and Gwinn, Michelle L. and Zhou, Liwei and Zafar, Nikhat and Khouri, Hoda and Radune, Diana and Dimitrov, George and Watkins, Kisha and O{\textquoteright}Connor, Kevin J. B. and Smith, Shannon and Utterback, Teresa R. and White, Owen and Rubens, Craig E. and Grandi, Guido and Madoff, Lawrence C. and Kasper, Dennis L. and Telford, John L. and Wessels, Michael R. and Rappuoli, Rino and Fraser, Claire M.} } @article {49637, title = {Transcriptional profiling of the hyperthermophilic methanarchaeon Methanococcus jannaschii in response to lethal heat and non-lethal cold shock.}, journal = {Environ Microbiol}, volume = {7}, year = {2005}, month = {2005 Jun}, pages = {789-97}, abstract = {

Temperature shock of the hyperthermophilic methanarchaeon Methanococcus jannaschii from its optimal growth temperature of 85 degrees C to 65 degrees C and 95 degrees C resulted in different transcriptional responses characteristic of both the direction of shock (heat or cold shock) and whether the shock was lethal. Specific outcomes of lethal heat shock to 95 degrees C included upregulation of genes encoding chaperones, and downregulation of genes encoding subunits of the H+ transporting ATP synthase. A gene encoding an alpha subunit of a putative prefoldin was also upregulated, which may comprise a novel element in the protein processing pathway in M. jannaschii. Very different responses were observed upon cold shock to 65 degrees C. These included upregulation of a gene encoding an RNA helicase and other genes involved in transcription and translation, and upregulation of genes coding for proteases and transport proteins. Also upregulated was a gene that codes for an 18 kDa FKBP-type PPIase, which may facilitate protein folding at low temperatures. Transcriptional profiling also revealed several hypothetical proteins that respond to temperature stress conditions.

}, keywords = {Adaptation, Physiological, Archaeal Proteins, Cold Temperature, Gene Expression Profiling, Gene Expression Regulation, Archaeal, Heat-Shock Proteins, Hot Temperature, Methanococcus, Temperature, Transcription, Genetic}, issn = {1462-2912}, doi = {10.1111/j.1462-2920.2005.00751.x}, author = {Boonyaratanakornkit, Boonchai B and Simpson, Anjana J and Whitehead, Timothy A and Fraser, Claire M and el-Sayed, Najib M A and Clark, Douglas S} } @article {38538, title = {Transcriptional profiling of the hyperthermophilic methanarchaeon Methanococcus jannaschii in response to lethal heat and non-lethal cold shock}, journal = {Environmental MicrobiologyEnvironmental Microbiology}, volume = {7}, year = {2005}, type = {10.1111/j.1462-2920.2005.00751.x}, abstract = {Temperature shock of the hyperthermophilic methanarchaeon Methanococcus jannaschii from its optimal growth temperature of 85{\textdegree}C to 65{\textdegree}C and 95{\textdegree}C resulted in different transcriptional responses characteristic of both the direction of shock (heat or cold shock) and whether the shock was lethal. Specific outcomes of lethal heat shock to 95{\textdegree}C included upregulation of genes encoding chaperones, and downregulation of genes encoding subunits of the H+ transporting ATP synthase. A gene encoding an α subunit of a putative prefoldin was also upregulated, which may comprise a novel element in the protein processing pathway in M. jannaschii. Very different responses were observed upon cold shock to 65{\textdegree}C. These included upregulation of a gene encoding an RNA helicase and other genes involved in transcription and translation, and upregulation of genes coding for proteases and transport proteins. Also upregulated was a gene that codes for an 18~kDa FKBP-type PPIase, which may facilitate protein folding at low temperatures. Transcriptional profiling also revealed several hypothetical proteins that respond to temperature stress conditions.}, isbn = {1462-2920}, author = {Boonyaratanakornkit, Boonchai B. and Simpson, Anjana J. and Whitehead, Timothy A. and Fraser, Claire M. and Najib M. El-Sayed and Clark, Douglas S.} } @article {38575, title = {Whole-genome sequence analysis of Pseudomonas syringae pv. phaseolicola 1448A reveals divergence among pathovars in genes involved in virulence and transposition}, journal = {Journal of bacteriologyJournal of bacteriology}, volume = {187}, year = {2005}, note = {http://www.ncbi.nlm.nih.gov/pubmed/16159782?dopt=Abstract}, type = {10.1128/JB.187.18.6488-6498.2005}, abstract = {Pseudomonas syringae pv. phaseolicola, a gram-negative bacterial plant pathogen, is the causal agent of halo blight of bean. In this study, we report on the genome sequence of P. syringae pv. phaseolicola isolate 1448A, which encodes 5,353 open reading frames (ORFs) on one circular chromosome (5,928,787 bp) and two plasmids (131,950 bp and 51,711 bp). Comparative analyses with a phylogenetically divergent pathovar, P. syringae pv. tomato DC3000, revealed a strong degree of conservation at the gene and genome levels. In total, 4,133 ORFs were identified as putative orthologs in these two pathovars using a reciprocal best-hit method, with 3,941 ORFs present in conserved, syntenic blocks. Although these two pathovars are highly similar at the physiological level, they have distinct host ranges; 1448A causes disease in beans, and DC3000 is pathogenic on tomato and Arabidopsis. Examination of the complement of ORFs encoding virulence, fitness, and survival factors revealed a substantial, but not complete, overlap between these two pathovars. Another distinguishing feature between the two pathovars is their distinctive sets of transposable elements. With access to a fifth complete pseudomonad genome sequence, we were able to identify 3,567 ORFs that likely comprise the core Pseudomonas genome and 365 ORFs that are P. syringae specific.}, keywords = {Bacterial Proteins, DNA, Bacterial, Genes, Bacterial, Genome, Bacterial, Molecular Sequence Data, Pseudomonas syringae, Species Specificity, virulence}, author = {Joardar, Vinita and Lindeberg, Magdalen and Jackson, Robert W. and J. Selengut and Dodson, Robert and Brinkac, Lauren M. and Daugherty, Sean C. and Deboy, Robert and Durkin, A. Scott and Giglio, Michelle Gwinn and Madupu, Ramana and Nelson, William C. and Rosovitz, M. J. and Sullivan, Steven and Crabtree, Jonathan and Creasy, Todd and Davidsen, Tanja and Haft, Dan H. and Zafar, Nikhat and Zhou, Liwei and Halpin, Rebecca and Holley, Tara and Khouri, Hoda and Feldblyum, Tamara and White, Owen and Fraser, Claire M. and Chatterjee, Arun K. and Cartinhour, Sam and Schneider, David J. and Mansfield, John and Collmer, Alan and Buell, C. Robin} } @article {38165, title = {Comparison of the genome of the oral pathogen Treponema denticola with other spirochete genomes}, journal = {Proceedings of the National Academy of Sciences of the United States of AmericaProceedings of the National Academy of Sciences of the United States of America}, volume = {101}, year = {2004}, note = {http://www.ncbi.nlm.nih.gov/pubmed/15064399?dopt=Abstract}, type = {10.1073/pnas.0307639101}, abstract = {We present the complete 2,843,201-bp genome sequence of Treponema denticola (ATCC 35405) an oral spirochete associated with periodontal disease. Analysis of the T. denticola genome reveals factors mediating coaggregation, cell signaling, stress protection, and other competitive and cooperative measures, consistent with its pathogenic nature and lifestyle within the mixed-species environment of subgingival dental plaque. Comparisons with previously sequenced spirochete genomes revealed specific factors contributing to differences and similarities in spirochete physiology as well as pathogenic potential. The T. denticola genome is considerably larger in size than the genome of the related syphilis-causing spirochete Treponema pallidum. The differences in gene content appear to be attributable to a combination of three phenomena: genome reduction, lineage-specific expansions, and horizontal gene transfer. Genes lost due to reductive evolution appear to be largely involved in metabolism and transport, whereas some of the genes that have arisen due to lineage-specific expansions are implicated in various pathogenic interactions, and genes acquired via horizontal gene transfer are largely phage-related or of unknown function.}, keywords = {ATP-Binding Cassette Transporters, Bacterial Proteins, Base Sequence, Borrelia burgdorferi, Genes, Bacterial, Genome, Bacterial, Leptospira interrogans, Models, Genetic, Molecular Sequence Data, Mouth, Sequence Homology, Amino Acid, Treponema, Treponema pallidum}, author = {Seshadri, Rekha and Myers, Garry S. A. and Tettelin, Herv{\'e} and Eisen, Jonathan A. and Heidelberg, John F. and Dodson, Robert J. and Davidsen, Tanja M. and DeBoy, Robert T. and Fouts, Derrick E. and Haft, Dan H. and J. Selengut and Ren, Qinghu and Brinkac, Lauren M. and Madupu, Ramana and Kolonay, Jamie and Durkin, A. Scott and Daugherty, Sean C. and Shetty, Jyoti and Shvartsbeyn, Alla and Gebregeorgis, Elizabeth and Geer, Keita and Tsegaye, Getahun and Malek, Joel and Ayodeji, Bola and Shatsman, Sofiya and McLeod, Michael P. and Smajs, David and Howell, Jerrilyn K. and Pal, Sangita and Amin, Anita and Vashisth, Pankaj and McNeill, Thomas Z. and Xiang, Qin and Sodergren, Erica and Baca, Ernesto and Weinstock, George M. and Norris, Steven J. and Fraser, Claire M. and Paulsen, Ian T.} } @inbook {38266, title = {Free-Living to Freewheeling: The Evolution of Vibrio cholerae from Innocence to Infamy}, booktitle = {Infectious Disease and Host-Pathogen EvolutionInfectious Disease and Host-Pathogen Evolution}, year = {2004}, publisher = {Cambridge University Press}, organization = {Cambridge University Press}, isbn = {9780521820660}, author = {Rita R. Colwell and Faruque, S. M. and Nair, G. B.}, editor = {Dronamraju, Krishna R.} } @article {49635, title = {Gene synteny and evolution of genome architecture in trypanosomatids.}, journal = {Mol Biochem Parasitol}, volume = {134}, year = {2004}, month = {2004 Apr}, pages = {183-91}, abstract = {

The trypanosomatid protozoa Trypanosoma brucei, Trypanosoma cruzi and Leishmania major are related human pathogens that cause markedly distinct diseases. Using information from genome sequencing projects currently underway, we have compared the sequences of large chromosomal fragments from each species. Despite high levels of divergence at the sequence level, these three species exhibit a striking conservation of gene order, suggesting that selection has maintained gene order among the trypanosomatids over hundreds of millions of years of evolution. The few sites of genome rearrangement between these species are marked by the presence of retrotransposon-like elements, suggesting that retrotransposons may have played an important role in shaping trypanosomatid genome organization. A degenerate retroelement was identified in L. major by examining the regions near breakage points of the synteny. This is the first such element found in L. major suggesting that retroelements were found in the common ancestor of all three species.

}, keywords = {Animals, Computational Biology, Evolution, Molecular, Gene Order, Genome, Protozoan, Genomics, Leishmania major, Multigene Family, Recombination, Genetic, Retroelements, Selection, Genetic, Synteny, Trypanosoma brucei brucei, Trypanosoma cruzi, Trypanosomatina}, issn = {0166-6851}, doi = {10.1016/j.molbiopara.2003.11.012}, author = {Ghedin, Elodie and Bringaud, Frederic and Peterson, Jeremy and Myler, Peter and Berriman, Matthew and Ivens, Alasdair and Andersson, Bj{\"o}rn and Bontempi, Esteban and Eisen, Jonathan and Angiuoli, Sam and Wanless, David and Von Arx, Anna and Murphy, Lee and Lennard, Nicola and Salzberg, Steven and Adams, Mark D and White, Owen and Hall, Neil and Stuart, Kenneth and Fraser, Claire M and el-Sayed, Najib M A} } @article {38302, title = {Genome sequence of Silicibacter pomeroyi reveals adaptations to the marine environment}, journal = {NatureNature}, volume = {432}, year = {2004}, note = {http://www.ncbi.nlm.nih.gov/pubmed/15602564?dopt=Abstract}, type = {10.1038/nature03170}, abstract = {Since the recognition of prokaryotes as essential components of the oceanic food web, bacterioplankton have been acknowledged as catalysts of most major biogeochemical processes in the sea. Studying heterotrophic bacterioplankton has been challenging, however, as most major clades have never been cultured or have only been grown to low densities in sea water. Here we describe the genome sequence of Silicibacter pomeroyi, a member of the marine Roseobacter clade (Fig. 1), the relatives of which comprise approximately 10-20\% of coastal and oceanic mixed-layer bacterioplankton. This first genome sequence from any major heterotrophic clade consists of a chromosome (4,109,442 base pairs) and megaplasmid (491,611 base pairs). Genome analysis indicates that this organism relies upon a lithoheterotrophic strategy that uses inorganic compounds (carbon monoxide and sulphide) to supplement heterotrophy. Silicibacter pomeroyi also has genes advantageous for associations with plankton and suspended particles, including genes for uptake of algal-derived compounds, use of metabolites from reducing microzones, rapid growth and cell-density-dependent regulation. This bacterium has a physiology distinct from that of marine oligotrophs, adding a new strategy to the recognized repertoire for coping with a nutrient-poor ocean.}, keywords = {Adaptation, Physiological, Carrier Proteins, Genes, Bacterial, Genome, Bacterial, marine biology, Molecular Sequence Data, Oceans and Seas, Phylogeny, plankton, RNA, Ribosomal, 16S, Roseobacter, Seawater}, author = {Moran, Mary Ann and Buchan, Alison and Gonz{\'a}lez, Jos{\'e} M. and Heidelberg, John F. and Whitman, William B. and Kiene, Ronald P. and Henriksen, James R. and King, Gary M. and Belas, Robert and Fuqua, Clay and Brinkac, Lauren and Lewis, Matt and Johri, Shivani and Weaver, Bruce and Pai, Grace and Eisen, Jonathan A. and Rahe, Elisha and Sheldon, Wade M. and Ye, Wenying and Miller, Todd R. and Carlton, Jane and Rasko, David A. and Paulsen, Ian T. and Ren, Qinghu and Daugherty, Sean C. and DeBoy, Robert T. and Dodson, Robert J. and Durkin, A. Scott and Madupu, Ramana and Nelson, William C. and Sullivan, Steven A. and Rosovitz, M. J. and Haft, Daniel H. and J. Selengut and Ward, Naomi} } @article {38303, title = {The genome sequence of the anaerobic, sulfate-reducing bacterium Desulfovibrio vulgaris Hildenborough}, journal = {Nature biotechnologyNature biotechnology}, volume = {22}, year = {2004}, note = {http://www.ncbi.nlm.nih.gov/pubmed/15077118?dopt=Abstract}, type = {10.1038/nbt959}, abstract = {Desulfovibrio vulgaris Hildenborough is a model organism for studying the energy metabolism of sulfate-reducing bacteria (SRB) and for understanding the economic impacts of SRB, including biocorrosion of metal infrastructure and bioremediation of toxic metal ions. The 3,570,858 base pair (bp) genome sequence reveals a network of novel c-type cytochromes, connecting multiple periplasmic hydrogenases and formate dehydrogenases, as a key feature of its energy metabolism. The relative arrangement of genes encoding enzymes for energy transduction, together with inferred cellular location of the enzymes, provides a basis for proposing an expansion to the {\textquoteright}hydrogen-cycling{\textquoteright} model for increasing energy efficiency in this bacterium. Plasmid-encoded functions include modification of cell surface components, nitrogen fixation and a type-III protein secretion system. This genome sequence represents a substantial step toward the elucidation of pathways for reduction (and bioremediation) of pollutants such as uranium and chromium and offers a new starting point for defining this organism{\textquoteright}s complex anaerobic respiration.}, keywords = {Desulfovibrio vulgaris, Energy Metabolism, Genome, Bacterial, Molecular Sequence Data}, author = {Heidelberg, John F. and Seshadri, Rekha and Haveman, Shelley A. and Hemme, Christopher L. and Paulsen, Ian T. and Kolonay, James F. and Eisen, Jonathan A. and Ward, Naomi and Methe, Barbara and Brinkac, Lauren M. and Daugherty, Sean C. and DeBoy, Robert T. and Dodson, Robert J. and Durkin, A. Scott and Madupu, Ramana and Nelson, William C. and Sullivan, Steven A. and Fouts, Derrick and Haft, Daniel H. and J. Selengut and Peterson, Jeremy D. and Davidsen, Tanja M. and Zafar, Nikhat and Zhou, Liwei and Radune, Diana and Dimitrov, George and Hance, Mark and Tran, Kevin and Khouri, Hoda and Gill, John and Utterback, Terry R. and Feldblyum, Tamara V. and Wall, Judy D. and Voordouw, Gerrit and Fraser, Claire M.} } @article {38514, title = {Structural flexibility in the Burkholderia mallei genome}, journal = {Proceedings of the National Academy of Sciences of the United States of AmericaProceedings of the National Academy of Sciences of the United States of America}, volume = {101}, year = {2004}, note = {http://www.ncbi.nlm.nih.gov/pubmed/15377793?dopt=Abstract}, type = {10.1073/pnas.0403306101}, abstract = {The complete genome sequence of Burkholderia mallei ATCC 23344 provides insight into this highly infectious bacterium{\textquoteright}s pathogenicity and evolutionary history. B. mallei, the etiologic agent of glanders, has come under renewed scientific investigation as a result of recent concerns about its past and potential future use as a biological weapon. Genome analysis identified a number of putative virulence factors whose function was supported by comparative genome hybridization and expression profiling of the bacterium in hamster liver in vivo. The genome contains numerous insertion sequence elements that have mediated extensive deletions and rearrangements of the genome relative to Burkholderia pseudomallei. The genome also contains a vast number (>12,000) of simple sequence repeats. Variation in simple sequence repeats in key genes can provide a mechanism for generating antigenic variation that may account for the mammalian host{\textquoteright}s inability to mount a durable adaptive immune response to a B. mallei infection.}, keywords = {Animals, Base Composition, Base Sequence, Burkholderia mallei, Chromosomes, Bacterial, Cricetinae, Genome, Bacterial, Glanders, Liver, Mesocricetus, Molecular Sequence Data, Multigene Family, Oligonucleotide Array Sequence Analysis, Open Reading Frames, virulence}, author = {Nierman, William C. and DeShazer, David and Kim, H. Stanley and Tettelin, Herv{\'e} and Nelson, Karen E. and Feldblyum, Tamara and Ulrich, Ricky L. and Ronning, Catherine M. and Brinkac, Lauren M. and Daugherty, Sean C. and Davidsen, Tanja D. and DeBoy, Robert T. and Dimitrov, George and Dodson, Robert J. and Durkin, A. Scott and Gwinn, Michelle L. and Haft, Daniel H. and Khouri, Hoda and Kolonay, James F. and Madupu, Ramana and Mohammoud, Yasmin and Nelson, William C. and Radune, Diana and Romero, Claudia M. and Sarria, Saul and J. Selengut and Shamblin, Christine and Sullivan, Steven A. and White, Owen and Yu, Yan and Zafar, Nikhat and Zhou, Liwei and Fraser, Claire M.} } @article {38574, title = {Whole genome comparisons of serotype 4b and 1/2a strains of the food-borne pathogen Listeria monocytogenes reveal new insights into the core genome components of this species}, journal = {Nucleic acids researchNucleic Acids Research}, volume = {32}, year = {2004}, note = {http://www.ncbi.nlm.nih.gov/pubmed/15115801?dopt=Abstract}, type = {10.1093/nar/gkh562}, abstract = {The genomes of three strains of Listeria monocytogenes that have been associated with food-borne illness in the USA were subjected to whole genome comparative analysis. A total of 51, 97 and 69 strain-specific genes were identified in L.monocytogenes strains F2365 (serotype 4b, cheese isolate), F6854 (serotype 1/2a, frankfurter isolate) and H7858 (serotype 4b, meat isolate), respectively. Eighty-three genes were restricted to serotype 1/2a and 51 to serotype 4b strains. These strain- and serotype-specific genes probably contribute to observed differences in pathogenicity, and the ability of the organisms to survive and grow in their respective environmental niches. The serotype 1/2a-specific genes include an operon that encodes the rhamnose biosynthetic pathway that is associated with teichoic acid biosynthesis, as well as operons for five glycosyl transferases and an adenine-specific DNA methyltransferase. A total of 8603 and 105 050 high quality single nucleotide polymorphisms (SNPs) were found on the draft genome sequences of strain H7858 and strain F6854, respectively, when compared with strain F2365. Whole genome comparative analyses revealed that the L.monocytogenes genomes are essentially syntenic, with the majority of genomic differences consisting of phage insertions, transposable elements and SNPs.}, keywords = {Base Composition, Chromosomes, Bacterial, DNA Transposable Elements, Food Microbiology, Genes, Bacterial, Genome, Bacterial, Genomics, Listeria monocytogenes, Meat, Open Reading Frames, Physical Chromosome Mapping, Polymorphism, Single Nucleotide, Prophages, Serotyping, Species Specificity, Synteny, virulence}, author = {Nelson, Karen E. and Fouts, Derrick E. and Mongodin, Emmanuel F. and Ravel, Jacques and DeBoy, Robert T. and Kolonay, James F. and Rasko, David A. and Angiuoli, Samuel V. and Gill, Steven R. and Paulsen, Ian T. and Peterson, Jeremy and White, Owen and Nelson, William C. and Nierman, William and Beanan, Maureen J. and Brinkac, Lauren M. and Daugherty, Sean C. and Dodson, Robert J. and Durkin, A. Scott and Madupu, Ramana and Haft, Daniel H. and J. Selengut and Van Aken, Susan and Khouri, Hoda and Fedorova, Nadia and Forberger, Heather and Tran, Bao and Kathariou, Sophia and Wonderling, Laura D. and Uhlich, Gaylen A. and Bayles, Darrell O. and Luchansky, John B. and Fraser, Claire M.} } @article {38576, title = {Whole-genome shotgun assembly and comparison of human genome assemblies}, journal = {Proceedings of the National Academy of Sciences of the United States of AmericaProceedings of the National Academy of Sciences of the United States of America}, volume = {101}, year = {2004}, publisher = {National Acad Sciences}, author = {Istrail, S. and Sutton, G. G. and Florea, L. and Halpern, A. L. and Mobarry, C. M. and Lippert, R. and Walenz, B. and Shatkay, H. and Dew, I. and Miller, J. R. and others,} } @article {38098, title = {A 4-Year Study of the Epidemiology of Vibrio Cholerae in Four Rural Areas of Bangladesh}, journal = {Journal of Infectious DiseasesJ Infect Dis.Journal of Infectious DiseasesJ Infect Dis.}, volume = {187}, year = {2003}, type = {10.1086/345865}, abstract = {How Vibrio cholerae spreads around the world and what determines its seasonal peaks in endemic areas are not known. These features of cholera have been hypothesized to be primarily the result of environmental factors associated with aquatic habitats that can now be identified. Since 1997, fortnightly surveillance in 4 widely separated geographic locations in Bangladesh has been performed to identify patients with cholera and to collect environmental data. A total of 5670 patients (53\% <5 years of age) have been studied; 14.3\% had cholera (10.4\% due to V. cholerae O1 El Tor, 3.8\% due to O139). Both serogroups were found in all locations; outbreaks were seasonal and often occurred simultaneously. Water-use patterns showed that bathing and washing clothes in tube-well water was significantly protective in two of the sites. These data will be correlated with environmental factors, to develop a model for prediction of cholera outbreaks}, isbn = {0022-1899, 1537-6613}, author = {Sack, R. Bradley and Siddique, A. Kasem and Longini, Ira M. and Nizam, Azhar and Yunus, Md and M. Sirajul Islam and Morris and Ali, Afsar and Huq, Anwar and Nair, G. Balakrish and Qadri, Firdausi and Faruque, Shah M. and Sack, David A. and Rita R. Colwell} } @article {38166, title = {Complete genome sequence and comparative analysis of the metabolically versatile Pseudomonas putida KT2440}, journal = {Environmental MicrobiologyEnvironmental Microbiology}, volume = {5}, year = {2003}, author = {Nelson, K. E. and Weinel, C. and Paulsen, I. T. and Dodson, R. J. and Hilbert, H. and Martins dos Santos, V. A. P. and Fouts, D. E. and Gill, S. R. and M. Pop and Holmes, M. and others,} } @article {38168, title = {The complete genome sequence of the Arabidopsis and tomato pathogen Pseudomonas syringae pv. tomato DC3000}, journal = {Proceedings of the National Academy of Sciences of the United States of AmericaProceedings of the National Academy of Sciences of the United States of America}, volume = {100}, year = {2003}, note = {http://www.ncbi.nlm.nih.gov/pubmed/12928499?dopt=Abstract}, type = {10.1073/pnas.1731982100}, abstract = {We report the complete genome sequence of the model bacterial pathogen Pseudomonas syringae pathovar tomato DC3000 (DC3000), which is pathogenic on tomato and Arabidopsis thaliana. The DC3000 genome (6.5 megabases) contains a circular chromosome and two plasmids, which collectively encode 5,763 ORFs. We identified 298 established and putative virulence genes, including several clusters of genes encoding 31 confirmed and 19 predicted type III secretion system effector proteins. Many of the virulence genes were members of paralogous families and also were proximal to mobile elements, which collectively comprise 7\% of the DC3000 genome. The bacterium possesses a large repertoire of transporters for the acquisition of nutrients, particularly sugars, as well as genes implicated in attachment to plant surfaces. Over 12\% of the genes are dedicated to regulation, which may reflect the need for rapid adaptation to the diverse environments encountered during epiphytic growth and pathogenesis. Comparative analyses confirmed a high degree of similarity with two sequenced pseudomonads, Pseudomonas putida and Pseudomonas aeruginosa, yet revealed 1,159 genes unique to DC3000, of which 811 lack a known function.}, keywords = {Arabidopsis, Base Sequence, Biological Transport, Genome, Bacterial, Lycopersicon esculentum, Molecular Sequence Data, Plant Growth Regulators, Plasmids, Pseudomonas, Reactive Oxygen Species, Siderophores, virulence}, author = {Buell, C. Robin and Joardar, Vinita and Lindeberg, Magdalen and J. Selengut and Paulsen, Ian T. and Gwinn, Michelle L. and Dodson, Robert J. and DeBoy, Robert T. and Durkin, A. Scott and Kolonay, James F. and Madupu, Ramana and Daugherty, Sean and Brinkac, Lauren and Beanan, Maureen J. and Haft, Daniel H. and Nelson, William C. and Davidsen, Tanja and Zafar, Nikhat and Zhou, Liwei and Liu, Jia and Yuan, Qiaoping and Khouri, Hoda and Fedorova, Nadia and Tran, Bao and Russell, Daniel and Berry, Kristi and Utterback, Teresa and Aken, Susan E. van and Feldblyum, Tamara V. and D{\textquoteright}Ascenzo, Mark and Deng, Wen-Ling and Ramos, Adela R. and Alfano, James R. and Cartinhour, Samuel and Chatterjee, Arun K. and Delaney, Terrence P. and Lazarowitz, Sondra G. and Martin, Gregory B. and Schneider, David J. and Tang, Xiaoyan and Bender, Carol L. and White, Owen and Fraser, Claire M. and Collmer, Alan} } @article {38214, title = {The dog genome: survey sequencing and comparative analysis}, journal = {ScienceScience}, volume = {301}, year = {2003}, publisher = {American Association for the Advancement of Science}, author = {Kirkness, E. F. and Bafna, V. and Halpern, A. L. and Levy, S. and Remington, K. and Rusch, D. B. and Delcher, A. L. and M. Pop and Wang, W. and Fraser, C. M. and others,} } @article {38228, title = {Emergence and Evolution of Vibrio Cholerae O139}, journal = {Proceedings of the National Academy of SciencesPNASProceedings of the National Academy of SciencesPNAS}, volume = {100}, year = {2003}, type = {10.1073/pnas.0337468100}, abstract = {The emergence of Vibrio cholerae O139 Bengal during 1992{\textendash}1993 was associated with large epidemics of cholera in India and Bangladesh and, initially, with a total displacement of the existing V. cholerae O1 strains. However, the O1 strains reemerged in 1994 and initiated a series of disappearance and reemergence of either of the two serogroups that was associated with temporal genetic and phenotypic changes sustained by the strains. Since the initial emergence of the O139 vibrios, new variants of the pathogen derived from multiple progenitors have been isolated and characterized. The clinical and epidemiological characteristics of these strains have been studied. Rapid genetic reassortment in O139 strains appears to be a response to the changing epidemiology of V. cholerae O1 and also a strategy for persistence in competition with strains of the O1 serogroup. The emergence of V. cholerae O139 has provided a unique opportunity to witness genetic changes in V. cholerae that may be associated with displacement of an existing serogroup by a newly emerging one and, thus, provide new insights into the epidemiology of cholera. The genetic changes and natural selection involving both environmental and host factors are likely to influence profoundly the genetics, epidemiology, and evolution of toxigenic V. cholerae, not only in the Ganges Delta region of India and Bangladesh, but also in other areas of endemic and epidemic cholera.}, isbn = {0027-8424, 1091-6490}, author = {Faruque, Shah M. and Sack, David A. and Sack, R. Bradley and Rita R. Colwell and Takeda, Yoshifumi and Nair, G. Balakrish} } @article {38291, title = {Genome of Geobacter sulfurreducens: metal reduction in subsurface environments}, journal = {Science (New York, N.Y.)Science (New York, N.Y.)}, volume = {302}, year = {2003}, note = {http://www.ncbi.nlm.nih.gov/pubmed/14671304?dopt=Abstract}, type = {10.1126/science.1088727}, abstract = {The complete genome sequence of Geobacter sulfurreducens, a delta-proteobacterium, reveals unsuspected capabilities, including evidence of aerobic metabolism, one-carbon and complex carbon metabolism, motility, and chemotactic behavior. These characteristics, coupled with the possession of many two-component sensors and many c-type cytochromes, reveal an ability to create alternative, redundant, electron transport networks and offer insights into the process of metal ion reduction in subsurface environments. As well as playing roles in the global cycling of metals and carbon, this organism clearly has the potential for use in bioremediation of radioactive metals and in the generation of electricity.}, keywords = {Acetates, Acetyl Coenzyme A, Aerobiosis, Anaerobiosis, Bacterial Proteins, Carbon, Chemotaxis, Chromosomes, Bacterial, Cytochromes c, Electron Transport, Energy Metabolism, Genes, Bacterial, Genes, Regulator, Genome, Bacterial, Geobacter, Hydrogen, Metals, Movement, Open Reading Frames, Oxidation-Reduction, Phylogeny}, author = {Meth{\'e}, B. A. and Nelson, K. E. and Eisen, J. A. and Paulsen, I. T. and Nelson, W. and Heidelberg, J. F. and Wu, D. and Wu, M. and Ward, N. and Beanan, M. J. and Dodson, R. J. and Madupu, R. and Brinkac, L. M. and Daugherty, S. C. and DeBoy, R. T. and Durkin, A. S. and Gwinn, M. and Kolonay, J. F. and Sullivan, S. A. and Haft, D. H. and J. Selengut and Davidsen, T. M. and Zafar, N. and White, O. and Tran, B. and Romero, C. and Forberger, H. A. and Weidman, J. and Khouri, H. and Feldblyum, T. V. and Utterback, T. R. and Van Aken, S. E. and Lovley, D. R. and Fraser, C. M.} } @article {38300, title = {The genome sequence of Bacillus anthracis Ames and comparison to closely related bacteria}, journal = {NatureNature}, volume = {423}, year = {2003}, note = {[eacute]
[Oslash]}, type = {10.1038/nature01586}, abstract = {Bacillus anthracis is an endospore-forming bacterium that causes inhalational anthrax1. Key virulence genes are found on plasmids (extra-chromosomal, circular, double-stranded DNA molecules) pXO1 (ref. 2) and pXO2 (ref. 3). To identify additional genes that might contribute to virulence, we analysed the complete sequence of the chromosome of B. anthracis Ames (about 5.23 megabases). We found several chromosomally encoded proteins that may contribute to pathogenicity{\textemdash}including haemolysins, phospholipases and iron acquisition functions{\textemdash}and identified numerous surface proteins that might be important targets for vaccines and drugs. Almost all these putative chromosomal virulence and surface proteins have homologues in Bacillus cereus, highlighting the similarity of B. anthracis to near-neighbours that are not associated with anthrax4. By performing a comparative genome hybridization of 19 B. cereus and Bacillus thuringiensis strains against a B. anthracis DNA microarray, we confirmed the general similarity of chromosomal genes among this group of close relatives. However, we found that the gene sequences of pXO1 and pXO2 were more variable between strains, suggesting plasmid mobility in the group. The complete sequence of B. anthracis is a step towards a better understanding of anthrax pathogenesis.}, isbn = {0028-0836}, author = {Read, Timothy D. and Peterson, Scott N. and Tourasse, Nicolas and Baillie, Les W. and Paulsen, Ian T. and Nelson, Karen E. and Tettelin, Herv and Fouts, Derrick E. and Eisen, Jonathan A. and Gill, Steven R. and Holtzapple, Erik K. and kstad, Ole Andreas and Helgason, Erlendur and Rilstone, Jennifer and Wu, Martin and Kolonay, James F. and Beanan, Maureen J. and Dodson, Robert J. and Brinkac, Lauren M. and Gwinn, Michelle and DeBoy, Robert T. and Madpu, Ramana and Daugherty, Sean C. and Durkin, A. Scott and Haft, Daniel H. and Nelson, William C. and Peterson, Jeremy D. and M. Pop and Khouri, Hoda M. and Radune, Diana and Benton, Jonathan L. and Mahamoud, Yasmin and Jiang, Lingxia and Hance, Ioana R. and Weidman, Janice F. and Berry, Kristi J. and Plaut, Roger D. and Wolf, Alex M. and Watkins, Kisha L. and Nierman, William C. and Hazen, Alyson and Cline, Robin and Redmond, Caroline and Thwaite, Joanne E. and White, Owen and Salzberg, Steven L. and Thomason, Brendan and Friedlander, Arthur M. and Koehler, Theresa M. and Hanna, Philip C. and Kolst, and Anne-Brit and Fraser, Claire M.} } @article {38424, title = {Pathogenic Potential of Environmental Vibrio Cholerae Strains Carrying Genetic Variants of the Toxin-Coregulated Pilus Pathogenicity Island}, journal = {Infection and ImmunityInfect. Immun.Infection and ImmunityInfect. Immun.}, volume = {71}, year = {2003}, type = {10.1128/IAI.71.2.1020-1025.2003}, abstract = {The major virulence factors of toxigenic Vibrio cholerae are cholera toxin (CT), which is encoded by a lysogenic bacteriophage (CTXΦ), and toxin-coregulated pilus (TCP), an essential colonization factor which is also the receptor for CTXΦ. The genes for the biosynthesis of TCP are part of a larger genetic element known as the TCP pathogenicity island. To assess their pathogenic potential, we analyzed environmental strains of V. cholerae carrying genetic variants of the TCP pathogenicity island for colonization of infant mice, susceptibility to CTXΦ, and diarrheagenicity in adult rabbits. Analysis of 14 environmental strains, including 3 strains carrying a new allele of the tcpA gene, 9 strains carrying a new allele of the toxT gene, and 2 strains carrying conventional tcpA and toxT genes, showed that all strains colonized infant mice with various efficiencies in competition with a control El Tor biotype strain of V. cholerae O1. Five of the 14 strains were susceptible to CTXΦ, and these transductants produced CT and caused diarrhea in adult rabbits. These results suggested that the new alleles of the tcpA and toxT genes found in environmental strains of V. cholerae encode biologically active gene products. Detection of functional homologs of the TCP island genes in environmental strains may have implications for understanding the origin and evolution of virulence genes of V. cholerae.}, isbn = {0019-9567, 1098-5522}, author = {Faruque, Shah M. and Kamruzzaman, M. and Meraj, Ismail M. and Chowdhury, Nityananda and Nair, G. Balakrish and Sack, R. Bradley and Rita R. Colwell and Sack, David A.} } @article {49633, title = {The sequence and analysis of Trypanosoma brucei chromosome II.}, journal = {Nucleic Acids Res}, volume = {31}, year = {2003}, month = {2003 Aug 15}, pages = {4856-63}, abstract = {

We report here the sequence of chromosome II from Trypanosoma brucei, the causative agent of African sleeping sickness. The 1.2-Mb pairs encode about 470 predicted genes organised in 17 directional clusters on either strand, the largest cluster of which has 92 genes lined up over a 284-kb region. An analysis of the GC skew reveals strand compositional asymmetries that coincide with the distribution of protein-coding genes, suggesting these asymmetries may be the result of transcription-coupled repair on coding versus non-coding strand. A 5-cM genetic map of the chromosome reveals recombinational {\textquoteright}hot{\textquoteright} and {\textquoteright}cold{\textquoteright} regions, the latter of which is predicted to include the putative centromere. One end of the chromosome consists of a 250-kb region almost exclusively composed of RHS (pseudo)genes that belong to a newly characterised multigene family containing a hot spot of insertion for retroelements. Interspersed with the RHS genes are a few copies of truncated RNA polymerase pseudogenes as well as expression site associated (pseudo)genes (ESAGs) 3 and 4, and 76 bp repeats. These features are reminiscent of a vestigial variant surface glycoprotein (VSG) gene expression site. The other end of the chromosome contains a 30-kb array of VSG genes, the majority of which are pseudogenes, suggesting that this region may be a site for modular de novo construction of VSG gene diversity during transposition/gene conversion events.

}, keywords = {Animals, Antigens, Protozoan, Chromosome mapping, Chromosomes, DNA, Protozoan, Gene Duplication, Genes, Protozoan, Molecular Sequence Data, Pseudogenes, Recombination, Genetic, Sequence Analysis, DNA, Trypanosoma brucei brucei}, issn = {1362-4962}, author = {el-Sayed, Najib M A and Ghedin, Elodie and Song, Jinming and MacLeod, Annette and Bringaud, Frederic and Larkin, Christopher and Wanless, David and Peterson, Jeremy and Hou, Lihua and Taylor, Sonya and Tweedie, Alison and Biteau, Nicolas and Khalak, Hanif G and Lin, Xiaoying and Mason, Tanya and Hannick, Linda and Caler, Elisabet and Blandin, Ga{\"e}lle and Bartholomeu, Daniella and Simpson, Anjana J and Kaul, Samir and Zhao, Hong and Pai, Grace and Van Aken, Susan and Utterback, Teresa and Haas, Brian and Koo, Hean L and Umayam, Lowell and Suh, Bernard and Gerrard, Caroline and Leech, Vanessa and Qi, Rong and Zhou, Shiguo and Schwartz, David and Feldblyum, Tamara and Salzberg, Steven and Tait, Andrew and Turner, C Michael R and Ullu, Elisabetta and White, Owen and Melville, Sara and Adams, Mark D and Fraser, Claire M and Donelson, John E} } @inbook {38153, title = {Combinatorial Algorithms for Design of DNA Arrays}, booktitle = {Chip TechnologyChip Technology}, series = {Advances in Biochemical Engineering/Biotechnology}, volume = {77}, year = {2002}, publisher = {Springer Berlin / Heidelberg}, organization = {Springer Berlin / Heidelberg}, abstract = {Optimal design of DNA arrays requires the development of algorithms with two-fold goals: reducing the effects caused by unintended illumination ( border length minimization problem ) and reducing the complexity of masks ( mask decomposition problem ). We describe algorithms that reduce the number of rectangles in mask decomposition by 20{\textendash}30\% as compared to a standard array design under the assumption that the arrangement of oligonucleotides on the array is fixed. This algorithm produces provably optimal solution for all studied real instances of array design. We also address the difficult problem of finding an arrangement which minimizes the border length and come up with a new idea of threading that significantly reduces the border length as compared to standard designs.}, isbn = {978-3-540-43215-9}, author = {Sridhar Hannenhalli and Hubbell, Earl and Lipshutz, Robert and Pevzner, Pavel}, editor = {Hoheisel, J{\"o}rg and Brazma, A. and B{\"u}ssow, K. and Cantor, C. and Christians, F. and Chui, G. and Diaz, R. and Drmanac, R. and Drmanac, S. and Eickhoff, H. and Fellenberg, K. and Sridhar Hannenhalli and Hoheisel, J. and Hou, A. and Hubbell, E. and Jin, H. and Jin, P. and Jurinke, C. and Konthur, Z. and K{\"o}ster, H. and Kwon, S. and Lacy, S. and Lehrach, H. and Lipshutz, R. and Little, D. and Lueking, A. and McGall, G. and Moeur, B. and Nordhoff, E. and Nyarsik, L. and Pevzner, P. and Robinson, A. and Sarkans, U. and Shafto, J. and Sohail, M. and Southern, E. and Swanson, D. and Ukrainczyk, T. and van den Boom, D. and Vilo, J. and Vingron, M. and Walter, G. and Xu, C.} } @article {38157, title = {Comparative Genome Sequencing for Discovery of Novel Polymorphisms in Bacillus Anthracis}, journal = {ScienceScienceScienceScience}, volume = {296}, year = {2002}, type = {10.1126/science.1071837}, abstract = {Comparison of the whole-genome sequence ofBacillus anthracis isolated from a victim of a recent bioterrorist anthrax attack with a reference reveals 60 new markers that include single nucleotide polymorphisms (SNPs), inserted or deleted sequences, and tandem repeats. Genome comparison detected four high-quality SNPs between the two sequenced B. anthracischromosomes and seven differences among different preparations of the reference genome. These markers have been tested on a collection of anthrax isolates and were found to divide these samples into distinct families. These results demonstrate that genome-based analysis of microbial pathogens will provide a powerful new tool for investigation of infectious disease outbreaks.}, isbn = {0036-8075, 1095-9203}, author = {Read, Timothy D. and Salzberg, Steven L. and M. Pop and Shumway, Martin and Umayam, Lowell and Jiang, Lingxia and Holtzapple, Erik and Busch, Joseph D. and Smith, Kimothy L. and Schupp, James M. and Solomon, Daniel and Keim, Paul and Fraser, Claire M.} } @article {49687, title = {The draft genome of Ciona intestinalis: insights into chordate and vertebrate origins.}, journal = {Science}, volume = {298}, year = {2002}, month = {2002 Dec 13}, pages = {2157-67}, abstract = {

The first chordates appear in the fossil record at the time of the Cambrian explosion, nearly 550 million years ago. The modern ascidian tadpole represents a plausible approximation to these ancestral chordates. To illuminate the origins of chordate and vertebrates, we generated a draft of the protein-coding portion of the genome of the most studied ascidian, Ciona intestinalis. The Ciona genome contains approximately 16,000 protein-coding genes, similar to the number in other invertebrates, but only half that found in vertebrates. Vertebrate gene families are typically found in simplified form in Ciona, suggesting that ascidians contain the basic ancestral complement of genes involved in cell signaling and development. The ascidian genome has also acquired a number of lineage-specific innovations, including a group of genes engaged in cellulose metabolism that are related to those in bacteria and fungi.

}, keywords = {Alleles, Animals, Apoptosis, Base Sequence, Cellulose, Central Nervous System, Ciona intestinalis, Computational Biology, Endocrine System, Gene Dosage, Gene Duplication, genes, Genes, Homeobox, Genome, Heart, Immunity, Molecular Sequence Data, Multigene Family, Muscle Proteins, Organizers, Embryonic, Phylogeny, Polymorphism, Genetic, Proteins, Sequence Analysis, DNA, Sequence Homology, Nucleic Acid, Species Specificity, Thyroid Gland, Urochordata, Vertebrates}, issn = {1095-9203}, doi = {10.1126/science.1080049}, author = {Dehal, Paramvir and Satou, Yutaka and Campbell, Robert K and Chapman, Jarrod and Degnan, Bernard and De Tomaso, Anthony and Davidson, Brad and Di Gregorio, Anna and Gelpke, Maarten and Goodstein, David M and Harafuji, Naoe and Hastings, Kenneth E M and Ho, Isaac and Hotta, Kohji and Huang, Wayne and Kawashima, Takeshi and Lemaire, Patrick and Martinez, Diego and Meinertzhagen, Ian A and Necula, Simona and Nonaka, Masaru and Putnam, Nik and Rash, Sam and Saiga, Hidetoshi and Satake, Masanobu and Terry, Astrid and Yamada, Lixy and Wang, Hong-Gang and Awazu, Satoko and Azumi, Kaoru and Boore, Jeffrey and Branno, Margherita and Chin-Bow, Stephen and DeSantis, Rosaria and Doyle, Sharon and Francino, Pilar and Keys, David N and Haga, Shinobu and Hayashi, Hiroko and Hino, Kyosuke and Imai, Kaoru S and Inaba, Kazuo and Kano, Shungo and Kobayashi, Kenji and Kobayashi, Mari and Lee, Byung-In and Makabe, Kazuhiro W and Manohar, Chitra and Matassi, Giorgio and Medina, Monica and Mochizuki, Yasuaki and Mount, Steve and Morishita, Tomomi and Miura, Sachiko and Nakayama, Akie and Nishizaka, Satoko and Nomoto, Hisayo and Ohta, Fumiko and Oishi, Kazuko and Rigoutsos, Isidore and Sano, Masako and Sasaki, Akane and Sasakura, Yasunori and Shoguchi, Eiichi and Shin-i, Tadasu and Spagnuolo, Antoinetta and Stainier, Didier and Suzuki, Miho M and Tassy, Olivier and Takatori, Naohito and Tokuoka, Miki and Yagi, Kasumi and Yoshizaki, Fumiko and Wada, Shuichi and Zhang, Cindy and Hyatt, P Douglas and Larimer, Frank and Detter, Chris and Doggett, Norman and Glavina, Tijana and Hawkins, Trevor and Richardson, Paul and Lucas, Susan and Kohara, Yuji and Levine, Michael and Satoh, Nori and Rokhsar, Daniel S} } @article {38295, title = {Genome sequence and comparative analysis of the model rodent malaria parasite Plasmodium yoelii yoelii}, journal = {NatureNature}, volume = {419}, year = {2002}, type = {10.1038/nature01099}, abstract = {Species of malaria parasite that infect rodents have long been used as models for malaria disease research. Here we report the whole-genome shotgun sequence of one species, Plasmodium yoelii yoelii, and comparative studies with the genome of the human malaria parasite Plasmodium falciparum clone 3D7. A synteny map of 2,212 P. y. yoelii contiguous DNA sequences (contigs) aligned to 14 P. falciparum chromosomes reveals marked conservation of gene synteny within the body of each chromosome. Of about 5,300 P. falciparum genes, more than 3,300 P. y. yoelii orthologues of predominantly metabolic function were identified. Over 800 copies of a variant antigen gene located in subtelomeric regions were found. This is the first genome sequence of a model eukaryotic parasite, and it provides insight into the use of such systems in the modelling of Plasmodium biology and disease.}, isbn = {0028-0836}, author = {Carlton, Jane M. and Angiuoli, Samuel V. and Suh, Bernard B. and Kooij, Taco W. and Pertea, Mihaela and Silva, Joana C. and Ermolaeva, Maria D. and Allen, Jonathan E. and J. Selengut and Koo, Hean L. and Peterson, Jeremy D. and M. Pop and Kosack, Daniel S. and Shumway, Martin F. and Bidwell, Shelby L. and Shallom, Shamira J. and Aken, Susan E. van and Riedmuller, Steven B. and Feldblyum, Tamara V. and Cho, Jennifer K. and Quackenbush, John and Sedegah, Martha and Shoaibi, Azadeh and Cummings, Leda M. and Florens, Laurence and Yates, John R. and Raine, J. Dale and Sinden, Robert E. and Harris, Michael A. and Cunningham, Deirdre A. and Preiser, Peter R. and Bergman, Lawrence W. and Vaidya, Akhil B. and Lin, Leo H. van and Janse, Chris J. and Waters, Andrew P. and Smith, Hamilton O. and White, Owen R. and Salzberg, Steven L. and Venter, J. Craig and Fraser, Claire M. and Hoffman, Stephen L. and Gardner, Malcolm J. and Carucci, Daniel J.} } @article {38304, title = {Genome sequence of the human malaria parasite Plasmodium falciparum}, journal = {NatureNature}, volume = {419}, year = {2002}, note = {http://www.ncbi.nlm.nih.gov/pubmed/12368864?dopt=Abstract}, type = {10.1038/nature01097}, abstract = {The parasite Plasmodium falciparum is responsible for hundreds of millions of cases of malaria, and kills more than one million African children annually. Here we report an analysis of the genome sequence of P. falciparum clone 3D7. The 23-megabase nuclear genome consists of 14 chromosomes, encodes about 5,300 genes, and is the most (A + T)-rich genome sequenced to date. Genes involved in antigenic variation are concentrated in the subtelomeric regions of the chromosomes. Compared to the genomes of free-living eukaryotic microbes, the genome of this intracellular parasite encodes fewer enzymes and transporters, but a large proportion of genes are devoted to immune evasion and host-parasite interactions. Many nuclear-encoded proteins are targeted to the apicoplast, an organelle involved in fatty-acid and isoprenoid metabolism. The genome sequence provides the foundation for future studies of this organism, and is being exploited in the search for new drugs and vaccines to fight malaria.}, keywords = {Animals, Chromosome Structures, DNA Repair, DNA Replication, DNA, Protozoan, Evolution, Molecular, Genome, Protozoan, HUMANS, Malaria Vaccines, Malaria, Falciparum, Membrane Transport Proteins, Molecular Sequence Data, Plasmodium falciparum, Plastids, Proteome, Protozoan Proteins, Recombination, Genetic, Sequence Analysis, DNA}, author = {Gardner, Malcolm J. and Hall, Neil and Fung, Eula and White, Owen and Berriman, Matthew and Hyman, Richard W. and Carlton, Jane M. and Pain, Arnab and Nelson, Karen E. and Bowman, Sharen and Paulsen, Ian T. and James, Keith and Eisen, Jonathan A. and Rutherford, Kim and Salzberg, Steven L. and Craig, Alister and Kyes, Sue and Chan, Man-Suen and Nene, Vishvanath and Shallom, Shamira J. and Suh, Bernard and Peterson, Jeremy and Angiuoli, Sam and Pertea, Mihaela and Allen, Jonathan and J. Selengut and Haft, Daniel and Mather, Michael W. and Vaidya, Akhil B. and Martin, David M. A. and Fairlamb, Alan H. and Fraunholz, Martin J. and Roos, David S. and Ralph, Stuart A. and McFadden, Geoffrey I. and Cummings, Leda M. and Subramanian, G. Mani and Mungall, Chris and Venter, J. Craig and Carucci, Daniel J. and Hoffman, Stephen L. and Newbold, Chris and Davis, Ronald W. and Fraser, Claire M. and Barrell, Bart} } @article {38492, title = {Sequence of Plasmodium falciparum chromosomes 2, 10, 11 and 14}, journal = {NatureNature}, volume = {419}, year = {2002}, note = {http://www.ncbi.nlm.nih.gov/pubmed/12368868?dopt=Abstract}, type = {10.1038/nature01094}, abstract = {The mosquito-borne malaria parasite Plasmodium falciparum kills an estimated 0.7-2.7 million people every year, primarily children in sub-Saharan Africa. Without effective interventions, a variety of factors-including the spread of parasites resistant to antimalarial drugs and the increasing insecticide resistance of mosquitoes-may cause the number of malaria cases to double over the next two decades. To stimulate basic research and facilitate the development of new drugs and vaccines, the genome of Plasmodium falciparum clone 3D7 has been sequenced using a chromosome-by-chromosome shotgun strategy. We report here the nucleotide sequences of chromosomes 10, 11 and 14, and a re-analysis of the chromosome 2 sequence. These chromosomes represent about 35\% of the 23-megabase P. falciparum genome.}, keywords = {Animals, Chromosomes, DNA, Protozoan, Genome, Protozoan, Plasmodium falciparum, Proteome, Protozoan Proteins, Sequence Analysis, DNA}, author = {Gardner, Malcolm J. and Shallom, Shamira J. and Carlton, Jane M. and Salzberg, Steven L. and Nene, Vishvanath and Shoaibi, Azadeh and Ciecko, Anne and Lynn, Jeffery and Rizzo, Michael and Weaver, Bruce and Jarrahi, Behnam and Brenner, Michael and Parvizi, Babak and Tallon, Luke and Moazzez, Azita and Granger, David and Fujii, Claire and Hansen, Cheryl and Pederson, James and Feldblyum, Tamara and Peterson, Jeremy and Suh, Bernard and Angiuoli, Sam and Pertea, Mihaela and Allen, Jonathan and J. Selengut and White, Owen and Cummings, Leda M. and Smith, Hamilton O. and Adams, Mark D. and Venter, J. Craig and Carucci, Daniel J. and Hoffman, Stephen L. and Fraser, Claire M.} } @conference {49569, title = {Automatically tracking and analyzing the behavior of live insect colonies}, booktitle = {the fifth international conferenceProceedings of the fifth international conference on Autonomous agents - AGENTS {\textquoteright}01}, year = {2001}, publisher = {ACM Press}, organization = {ACM Press}, address = {Montreal, Quebec, CanadaNew York, New York, USA}, isbn = {158113326X}, doi = {10.1145/37573510.1145/375735.376434}, url = {http://portal.acm.org/citation.cfm?doid=375735http://portal.acm.org/citation.cfm?doid=375735.376434}, author = {Balch, Tucker and Khan, Zia and Veloso, Manuela} } @article {49692, title = {The genome sequence of Drosophila melanogaster.}, journal = {Science}, volume = {287}, year = {2000}, month = {2000 Mar 24}, pages = {2185-95}, abstract = {

The fly Drosophila melanogaster is one of the most intensively studied organisms in biology and serves as a model system for the investigation of many developmental and cellular processes common to higher eukaryotes, including humans. We have determined the nucleotide sequence of nearly all of the approximately 120-megabase euchromatic portion of the Drosophila genome using a whole-genome shotgun sequencing strategy supported by extensive clone-based sequence and a high-quality bacterial artificial chromosome physical map. Efforts are under way to close the remaining gaps; however, the sequence is of sufficient accuracy and contiguity to be declared substantially complete and to support an initial analysis of genome structure and preliminary gene annotation and interpretation. The genome encodes approximately 13,600 genes, somewhat fewer than the smaller Caenorhabditis elegans genome, but with comparable functional diversity.

}, keywords = {Animals, Biological Transport, Chromatin, Cloning, Molecular, Computational Biology, Contig Mapping, Cytochrome P-450 Enzyme System, DNA Repair, DNA Replication, Drosophila melanogaster, Euchromatin, Gene Library, Genes, Insect, Genome, Heterochromatin, Insect Proteins, Nuclear Proteins, Protein Biosynthesis, Sequence Analysis, DNA, Transcription, Genetic}, issn = {0036-8075}, author = {Adams, M D and Celniker, S E and Holt, R A and Evans, C A and Gocayne, J D and Amanatides, P G and Scherer, S E and Li, P W and Hoskins, R A and Galle, R F and George, R A and Lewis, S E and Richards, S and Ashburner, M and Henderson, S N and Sutton, G G and Wortman, J R and Yandell, M D and Zhang, Q and Chen, L X and Brandon, R C and Rogers, Y H and Blazej, R G and Champe, M and Pfeiffer, B D and Wan, K H and Doyle, C and Baxter, E G and Helt, G and Nelson, C R and Gabor, G L and Abril, J F and Agbayani, A and An, H J and Andrews-Pfannkoch, C and Baldwin, D and Ballew, R M and Basu, A and Baxendale, J and Bayraktaroglu, L and Beasley, E M and Beeson, K Y and Benos, P V and Berman, B P and Bhandari, D and Bolshakov, S and Borkova, D and Botchan, M R and Bouck, J and Brokstein, P and Brottier, P and Burtis, K C and Busam, D A and Butler, H and Cadieu, E and Center, A and Chandra, I and Cherry, J M and Cawley, S and Dahlke, C and Davenport, L B and Davies, P and de Pablos, B and Delcher, A and Deng, Z and Mays, A D and Dew, I and Dietz, S M and Dodson, K and Doup, L E and Downes, M and Dugan-Rocha, S and Dunkov, B C and Dunn, P and Durbin, K J and Evangelista, C C and Ferraz, C and Ferriera, S and Fleischmann, W and Fosler, C and Gabrielian, A E and Garg, N S and Gelbart, W M and Glasser, K and Glodek, A and Gong, F and Gorrell, J H and Gu, Z and Guan, P and Harris, M and Harris, N L and Harvey, D and Heiman, T J and Hernandez, J R and Houck, J and Hostin, D and Houston, K A and Howland, T J and Wei, M H and Ibegwam, C and Jalali, M and Kalush, F and Karpen, G H and Ke, Z and Kennison, J A and Ketchum, K A and Kimmel, B E and Kodira, C D and Kraft, C and Kravitz, S and Kulp, D and Lai, Z and Lasko, P and Lei, Y and Levitsky, A A and Li, J and Li, Z and Liang, Y and Lin, X and Liu, X and Mattei, B and McIntosh, T C and McLeod, M P and McPherson, D and Merkulov, G and Milshina, N V and Mobarry, C and Morris, J and Moshrefi, A and Mount, S M and Moy, M and Murphy, B and Murphy, L and Muzny, D M and Nelson, D L and Nelson, D R and Nelson, K A and Nixon, K and Nusskern, D R and Pacleb, J M and Palazzolo, M and Pittman, G S and Pan, S and Pollard, J and Puri, V and Reese, M G and Reinert, K and Remington, K and Saunders, R D and Scheeler, F and Shen, H and Shue, B C and Sid{\'e}n-Kiamos, I and Simpson, M and Skupski, M P and Smith, T and Spier, E and Spradling, A C and Stapleton, M and Strong, R and Sun, E and Svirskas, R and Tector, C and Turner, R and Venter, E and Wang, A H and Wang, X and Wang, Z Y and Wassarman, D A and Weinstock, G M and Weissenbach, J and Williams, S M and Worley, K C and Wu, D and Yang, S and Yao, Q A and Ye, J and Yeh, R F and Zaveri, J S and Zhan, M and Zhang, G and Zhao, Q and Zheng, L and Zheng, X H and Zhong, F N and Zhong, W and Zhou, X and Zhu, S and Zhu, X and Smith, H O and Gibbs, R A and Myers, E W and Rubin, G M and Venter, J C} } @article {38434, title = {Phylogenetic relationships of {\i}t Phytophthora species based on ribosomal ITS I DNA sequence analysis with emphasis on Waterhouse groups V and VI}, journal = {Mycol ResMycol Res}, volume = {104}, year = {2000}, abstract = {Phylogenetic relationships among Phytophthora species were investigated by sequence analysis of the internal transcribed spacer region I of the ribosomal DNA repeat unit. The extensive collection of isolates included taxa from all six morphological groups recognized by Waterhouse (1963) including molecular groups previously identified using isozymes and mtDNA restriction fragment length polymorphisms. Similar to previous studies, the inferred relationships indicated that molecular groups of P. cryptooea/drechsleri-like and P. megasperma-like taxa are polyphyletic. Morphological groups V and VI, which are differentiated by the presence of amphigynous or paragynous antheridia, are not monophyletic: species of the two groups are interspersed in the tree. Species with papillate and semi-papillate sporangia (groups I-IV) clustered together and this cluster was distinct from those of species with non-papillate sporangia. There was no congruence between the mode of antheridial attachment, sporangial caducity, or homo- or heterothallic habit and the molecular grouping of the species. Our study provides evidence that the antheridial position together with homo- or heterothallic habit does not reflect phylogenetic relationships within Phytophthora. Consequently, confirming studies done previously (Cooke \& Duncan 1997), this study provides evidence that the morphological characters used in Phytophthora taxonomy are of limited value for deducing phylogenetic relationships, because they exhibit convergent evolution.}, author = {F{\"o}rster, H. and Michael P. Cummings and Coffey, M. D.} } @article {38126, title = {Bacterial Start Site Prediction}, journal = {Nucleic Acids ResearchNucl. Acids Res.Nucleic Acids ResearchNucl. Acids Res.}, volume = {27}, year = {1999}, type = {10.1093/nar/27.17.3577}, abstract = {With the growing number of completely sequenced bacterial genes, accurate gene prediction in bacterial genomes remains an important problem. Although the existing tools predict genes in bacterial genomes with high overall accuracy, their ability to pinpoint the translation start site remains unsatisfactory. In this paper, we present a novel approach to bacterial start site prediction that takes into account multiple features of a potential start site, viz., ribosome binding site (RBS) binding energy, distance of the RBS from the start codon, distance from the beginning of the maximal ORF to the start codon, the start codon itself and the coding/non-coding potential around the start site. Mixed integer programing was used to optimize the discriminatory system. The accuracy of this approach is up to 90\%, compared to 70\%, using the most common tools in fully automated mode (that is, without expert human post-processing of results). The approach is evaluated using Bacillus subtilis, Escherichia coli and Pyrococcus furiosus. These three genomes cover a broad spectrum of bacterial genomes, since B.subtilis is a Gram-positive bacterium, E.coli is a Gram-negative bacterium and P.furiosus is an archaebacterium. A significant problem is generating a set of {\textquoteleft}true{\textquoteright} start sites for algorithm training, in the absence of experimental work. We found that sequence conservation between P.furiosus and the related Pyrococcus horikoshii clearly delimited the gene start in many cases, providing a sufficient training set.}, isbn = {0305-1048, 1362-4962}, author = {Sridhar Hannenhalli and Hayes, William S. and Hatzigeorgiou, Artemis G. and Fickett, James W.} } @article {49627, title = {Genetic nomenclature for Trypanosoma and Leishmania.}, journal = {Mol Biochem Parasitol}, volume = {97}, year = {1998}, month = {1998 Nov 30}, pages = {221-4}, keywords = {Animals, Leishmania, Terminology as Topic, Trypanosoma}, issn = {0166-6851}, author = {Clayton, C and Adams, M and Almeida, R and Baltz, T and Barrett, M and Bastien, P and Belli, S and Beverley, S and Biteau, N and Blackwell, J and Blaineau, C and Boshart, M and Bringaud, F and Cross, G and Cruz, A and Degrave, W and Donelson, J and El-Sayed, N and Fu, G and Ersfeld, K and Gibson, W and Gull, K and Ivens, A and Kelly, J and Vanhamme, L} } @article {38548, title = {Trends in the early careers of life scientists - Preface and executive summary}, journal = {Mol Biol CellMol Biol Cell}, volume = {9}, year = {1998}, author = {Tilghman, S. and Astin, H. S. and Brinkley, W. and Chilton, M. D. and Michael P. Cummings and Ehrenberg, R. G. and Fox, M. F. and Glenn, K. and Green, P. J. and Hans, S. and Kelman, A. and LaPidus, J. and Levin, B. and McIntosh, J. R. and Riecken, H. and Stephen, P. E.} } @article {38361, title = {Local rules for protein folding on a triangular lattice and generalized hydrophobicity in the HP model}, journal = {Journal of Computational BiologyJournal of Computational Biology}, volume = {4}, year = {1997}, author = {Agarwala, R. and Batzoglou, S. and Dan{\v C}{\'I}K, V. and Decatur, S. E. and Sridhar Hannenhalli and Farach, M. and Muthukrishnan, S. and Skiena, S.} } @article {38442, title = {Positional sequencing by hybridization}, journal = {Computer applications in the biosciences : CABIOSComputer applications in the biosciences : CABIOS}, volume = {12}, year = {1996}, type = {10.1093/bioinformatics/12.1.19}, abstract = {Sequencing by hybridization (SBH) is a promising alternative to the classical DNA sequencing approaches. However, the resolving power of SBH is rather low: with 64kb sequencing chips, unknown DNA fragments only as long as 200 bp can be reconstructed in a single SBH experiment. To improve the resolving power of SBH, positional SBH (PSBH) has recently been suggested; this allows (with additional experimental work) approximate positions of every l-tuple in a target DNA fragment to be measured. We study the positional Eulerian path problem motivated by PSBH. The input to the positional eulerian path problem is an Eulerian graph G( V, E) in which every edge has an associated range of integers and the problem is to find an Eulerian path el, {\textellipsis}, e|E| in G such that the range of ei, contains i. We show that the positional Eulerian path problem is NP-complete even when the maximum out-degree (in-degree) of any vertex in the graph is 2. On a positive note we present polynomial algorithms to solve a special case of PSBH (bounded PSBH), where the range of the allowed positions for any edge is bounded by a constant (it corresponds to accurate experimental measurements of positions in PSBH). Moreover, if the positions of every l-tuple in an unknown DNA fragment of length n are measured with O(log n) error, then our algorithm runs in polynomial time. We also present an estimate of the resolving power of PSBH for a more realistic case when positions are measured with Θ(n) error.}, author = {Sridhar Hannenhalli and Feldman, William and Lewis, Herbert F. and Skiena, Steven S. and Pevzner, Pavel A.} } @article {38189, title = {Crystallization and preliminary X-ray investigation of the recombinant Trypanosoma brucei rhodesiense calmodulin}, journal = {Proteins: Structure, Function, and BioinformaticsProteins: Structure, Function, and Bioinformatics}, volume = {21}, year = {1995}, author = {Najib M. El-Sayed and Patton, C. L. and Harkins, P. C. and Fox, R. O. and Anderson, K.} } @article {49702, title = {Splicing signals in Drosophila: intron size, information content, and consensus sequences.}, journal = {Nucleic Acids Res}, volume = {20}, year = {1992}, month = {1992 Aug 25}, pages = {4255-62}, abstract = {

A database of 209 Drosophila introns was extracted from Genbank (release number 64.0) and examined by a number of methods in order to characterize features that might serve as signals for messenger RNA splicing. A tight distribution of sizes was observed: while the smallest introns in the database are 51 nucleotides, more than half are less than 80 nucleotides in length, and most of these have lengths in the range of 59-67 nucleotides. Drosophila splice sites found in large and small introns differ in only minor ways from each other and from those found in vertebrate introns. However, larger introns have greater pyrimidine-richness in the region between 11 and 21 nucleotides upstream of 3{\textquoteright} splice sites. The Drosophila branchpoint consensus matrix resembles C T A A T (in which branch formation occurs at the underlined A), and differs from the corresponding mammalian signal in the absence of G at the position immediately preceding the branchpoint. The distribution of occurrences of this sequence suggests a minimum distance between 5{\textquoteright} splice sites and branchpoints of about 38 nucleotides, and a minimum distance between 3{\textquoteright} splice sites and branchpoints of 15 nucleotides. The methods we have used detect no information in exon sequences other than in the few nucleotides immediately adjacent to the splice sites. However, Drosophila resembles many other species in that there is a discontinuity in A + T content between exons and introns, which are A + T rich.

}, keywords = {Animals, Base Sequence, Consensus Sequence, Databases, Factual, Drosophila, Introns, Molecular Sequence Data, RNA Splicing, RNA, Messenger, software}, issn = {0305-1048}, author = {Mount, S M and Burks, C and Hertz, G and Stormo, G D and White, O and Fields, C} } @article {38240, title = {Evolution of avocados as revealed by DNA restriction fragment variation}, journal = {J HeredJ Hered}, volume = {81}, year = {1990}, abstract = {Individuals representing the genus {\i}t Persea, subgenus {\i}t Persea were assayed for restriction fragment length polymorphisms in their chloroplast genome, nuclear ribosomal DNA, and the genes coding for the enzyme cellulase. The subgenus {\i}t Persea appears to consist of {\i}t P. schiedeana and a separate taxon containing the remaining species. {\i}t P. americana does not appear to be a monophyletic group. If {\i}t P. americana is to be maintained as a species containing var. {\i}t americana, var. {\i}t drymifolia, and var. {\i}t guatemalensis, then our data suggest that it should also contain varieties corresponding to {\i}t P. floccosa, {\i}t P. nubigena, and {\i}t P. steyermarkii. {\i}t P. americana var. {\i}t guatemalensis appears to have originated as a hybrid between {\i}t P. steyermarkii and {\i}t P. nubigena. The root-rot-resistant cultivar G755A is a hybrid progeny of {\i}t P. schiedeana and {\i}t P. americana var. guatemalensis. The three varieties of {\i}t P. americana were all distinguished by mutations.}, author = {Furnier, G. R. and Michael P. Cummings and Clegg, M. T.} }