@article {49623, title = {Bayesian integration of genetics and epigenetics detects causal regulatory SNPs underlying expression variability}, journal = {Nature Communications}, volume = {6}, year = {2015}, month = {Dec-10-2015}, pages = {8555}, doi = {10.1038/ncomms9555}, url = {http://www.nature.com/doifinder/10.1038/ncomms9555}, author = {Das, Avinash and Morley, Michael and Moravec, Christine S. and Tang, W. H. W. and Hakonarson, Hakon and Ashley, Euan A. and Brandimarto, Jeffrey and Hu, Ray and Li, Mingyao and Li, Hongzhe and Liu, Yichuan and Qu, Liming and Sanchez, Pablo and Margulies, Kenneth B. and Cappola, Thomas P. and Jensen, Shane and Hannenhalli, Sridhar} } @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 {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 {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 {38462, title = {Resistin gene variation is associated with systemic inflammation but not plasma adipokine levels, metabolic syndrome or coronary atherosclerosis in nondiabetic Caucasians}, journal = {Clinical EndocrinologyClinical Endocrinology}, volume = {70}, year = {2009}, type = {10.1111/j.1365-2265.2008.03375.x}, abstract = {Objective Resistin causes insulin resistance and diabetes in mice whereas in humans it is linked to inflammation and atherosclerosis. Few human genetic studies of resistin in inflammation and atherosclerosis have been performed. We hypothesized that the {\textendash}420C>G putative gain-of-function resistin variant would be associated with inflammatory markers and atherosclerosis but not with metabolic syndrome or adipokines in humans.Design and methods We examined the association of three resistin polymorphisms, {\textendash}852A>G, {\textendash}420C>G and +157C>T, and related haplotypes with plasma resistin, cytokines, C-reactive protein (CRP), adipokines, plasma lipoproteins, metabolic syndrome and coronary artery calcification (CAC) in nondiabetic Caucasians (n~=~851). Results Resistin levels were higher, dose-dependently, with the {\textendash}420G allele (CC 5{\textperiodcentered}9~{\textpm}~2{\textperiodcentered}7~ng/ml, GC 6{\textperiodcentered}5~{\textpm}~4{\textperiodcentered}0~ng/ml and GG 7{\textperiodcentered}2~{\textpm}~4{\textperiodcentered}8~ng/ml, trend P~=~0{\textperiodcentered}04) after age and gender adjustment [fold higher for GC~+~GG vs. CC; 1{\textperiodcentered}07~(1{\textperiodcentered}00{\textendash}1{\textperiodcentered}15), P~<~0{\textperiodcentered}05)]. The {\textendash}852A>G single nucleotide polymorphism (SNP) was associated with higher soluble tumour necrosis factor-receptor~2 (sol-TNFR2) levels in fully adjusted models [1{\textperiodcentered}06~(95\%~CI 1{\textperiodcentered}01{\textendash}1{\textperiodcentered}11), P~=~0{\textperiodcentered}01)]. The estimated resistin haplotype (GGT) was associated with sol-TNFR2 (P~=~0{\textperiodcentered}04) and the AGT haplotype was related to CRP (P~=~0{\textperiodcentered}04) in the fully adjusted models. Resistin SNPs and haplotypes were not associated with body mass index (BMI), fasting glucose, insulin resistance, metabolic syndrome, adipokines or CAC scores. Conclusions Despite modest associations with plasma resistin and inflammatory biomarkers, resistin 5' variants were not associated with metabolic parameters or coronary calcification. This suggests that resistin is an inflammatory cytokine in humans but has little influence on adiposity, metabolic syndrome or atherosclerosis.}, isbn = {1365-2265}, author = {Qasim, Atif N. and Metkus, Thomas S. and Tadesse, Mahlet and Lehrke, Michael and Restine, Stephanie and Wolfe, Megan L. and Sridhar Hannenhalli and Cappola, Thomas and Rader, Daniel J. and Reilly, Muredach P.} } @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 {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 {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 {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} } @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 {38105, title = {The African trypanosome genome}, journal = {International Journal for ParasitologyInternational Journal for Parasitology}, volume = {30}, year = {2000}, type = {16/S0020-7519(00)00015-1}, abstract = {The haploid nuclear genome of the African trypanosome, Trypanosoma brucei, is about 35 Mb and varies in size among different trypanosome isolates by as much as 25\%. The nuclear DNA of this diploid organism is distributed among three size classes of chromosomes: the megabase chromosomes of which there are at least 11 pairs ranging from 1 Mb to more than 6 Mb (numbered I-XI from smallest to largest); several intermediate chromosomes of 200-900 kb and uncertain ploidy; and about 100 linear minichromosomes of 50-150 kb. Size differences of as much as four-fold can occur, both between the two homologues of a megabase chromosome pair in a specific trypanosome isolate and among chromosome pairs in different isolates. The genomic DNA sequences determined to date indicated that about 50\% of the genome is coding sequence. The chromosomal telomeres possess TTAGGG repeats and many, if not all, of the telomeres of the megabase and intermediate chromosomes are linked to expression sites for genes encoding variant surface glycoproteins (VSGs). The minichromosomes serve as repositories for VSG genes since some but not all of their telomeres are linked to unexpressed VSG genes. A gene discovery program, based on sequencing the ends of cloned genomic DNA fragments, has generated more than 20 Mb of discontinuous single-pass genomic sequence data during the past year, and the complete sequences of chromosomes I and II (about 1 Mb each) in T. brucei GUTat 10.1 are currently being determined. It is anticipated that the entire genomic sequence of this organism will be known in a few years. Analysis of a test microarray of 400 cDNAs and small random genomic DNA fragments probed with RNAs from two developmental stages of T. brucei demonstrates that the microarray technology can be used to identify batteries of genes differentially expressed during the various life cycle stages of this parasite.}, isbn = {0020-7519}, author = {Najib M. El-Sayed and Hegde, Priti and Quackenbush, John and Melville, Sara E. and Donelson, John E.} }