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  • 1
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    The genome sequence of taurine cattle: a window to ruminant biology and evolution (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-25
    Description: To understand the biology and evolution of ruminants, the cattle genome was sequenced to about sevenfold coverage. The cattle genome contains a minimum of 22,000 genes, with a core set of 14,345 orthologs shared among seven mammalian species of which 1217 are absent or undetected in noneutherian (marsupial or monotreme) genomes. Cattle-specific evolutionary breakpoint regions in chromosomes have a higher density of segmental duplications, enrichment of repetitive elements, and species-specific variations in genes associated with lactation and immune responsiveness. Genes involved in metabolism are generally highly conserved, although five metabolic genes are deleted or extensively diverged from their human orthologs. The cattle genome sequence thus provides a resource for understanding mammalian evolution and accelerating livestock genetic improvement for milk and meat production.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2943200/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2943200/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bovine Genome Sequencing and Analysis Consortium -- Elsik, Christine G -- Tellam, Ross L -- Worley, Kim C -- Gibbs, Richard A -- Muzny, Donna M -- Weinstock, George M -- Adelson, David L -- Eichler, Evan E -- Elnitski, Laura -- Guigo, Roderic -- Hamernik, Debora L -- Kappes, Steve M -- Lewin, Harris A -- Lynn, David J -- Nicholas, Frank W -- Reymond, Alexandre -- Rijnkels, Monique -- Skow, Loren C -- Zdobnov, Evgeny M -- Schook, Lawrence -- Womack, James -- Alioto, Tyler -- Antonarakis, Stylianos E -- Astashyn, Alex -- Chapple, Charles E -- Chen, Hsiu-Chuan -- Chrast, Jacqueline -- Camara, Francisco -- Ermolaeva, Olga -- Henrichsen, Charlotte N -- Hlavina, Wratko -- Kapustin, Yuri -- Kiryutin, Boris -- Kitts, Paul -- Kokocinski, Felix -- Landrum, Melissa -- Maglott, Donna -- Pruitt, Kim -- Sapojnikov, Victor -- Searle, Stephen M -- Solovyev, Victor -- Souvorov, Alexandre -- Ucla, Catherine -- Wyss, Carine -- Anzola, Juan M -- Gerlach, Daniel -- Elhaik, Eran -- Graur, Dan -- Reese, Justin T -- Edgar, Robert C -- McEwan, John C -- Payne, Gemma M -- Raison, Joy M -- Junier, Thomas -- Kriventseva, Evgenia V -- Eyras, Eduardo -- Plass, Mireya -- Donthu, Ravikiran -- Larkin, Denis M -- Reecy, James -- Yang, Mary Q -- Chen, Lin -- Cheng, Ze -- Chitko-McKown, Carol G -- Liu, George E -- Matukumalli, Lakshmi K -- Song, Jiuzhou -- Zhu, Bin -- Bradley, Daniel G -- Brinkman, Fiona S L -- Lau, Lilian P L -- Whiteside, Matthew D -- Walker, Angela -- Wheeler, Thomas T -- Casey, Theresa -- German, J Bruce -- Lemay, Danielle G -- Maqbool, Nauman J -- Molenaar, Adrian J -- Seo, Seongwon -- Stothard, Paul -- Baldwin, Cynthia L -- Baxter, Rebecca -- Brinkmeyer-Langford, Candice L -- Brown, Wendy C -- Childers, Christopher P -- Connelley, Timothy -- Ellis, Shirley A -- Fritz, Krista -- Glass, Elizabeth J -- Herzig, Carolyn T A -- Iivanainen, Antti -- Lahmers, Kevin K -- Bennett, Anna K -- Dickens, C Michael -- Gilbert, James G R -- Hagen, Darren E -- Salih, Hanni -- Aerts, Jan -- Caetano, Alexandre R -- Dalrymple, Brian -- Garcia, Jose Fernando -- Gill, Clare A -- Hiendleder, Stefan G -- Memili, Erdogan -- Spurlock, Diane -- Williams, John L -- Alexander, Lee -- Brownstein, Michael J -- Guan, Leluo -- Holt, Robert A -- Jones, Steven J M -- Marra, Marco A -- Moore, Richard -- Moore, Stephen S -- Roberts, Andy -- Taniguchi, Masaaki -- Waterman, Richard C -- Chacko, Joseph -- Chandrabose, Mimi M -- Cree, Andy -- Dao, Marvin Diep -- Dinh, Huyen H -- Gabisi, Ramatu Ayiesha -- Hines, Sandra -- Hume, Jennifer -- Jhangiani, Shalini N -- Joshi, Vandita -- Kovar, Christie L -- Lewis, Lora R -- Liu, Yih-Shin -- Lopez, John -- Morgan, Margaret B -- Nguyen, Ngoc Bich -- Okwuonu, Geoffrey O -- Ruiz, San Juana -- Santibanez, Jireh -- Wright, Rita A -- Buhay, Christian -- Ding, Yan -- Dugan-Rocha, Shannon -- Herdandez, Judith -- Holder, Michael -- Sabo, Aniko -- Egan, Amy -- Goodell, Jason -- Wilczek-Boney, Katarzyna -- Fowler, Gerald R -- Hitchens, Matthew Edward -- Lozado, Ryan J -- Moen, Charles -- Steffen, David -- Warren, James T -- Zhang, Jingkun -- Chiu, Readman -- Schein, Jacqueline E -- Durbin, K James -- Havlak, Paul -- Jiang, Huaiyang -- Liu, Yue -- Qin, Xiang -- Ren, Yanru -- Shen, Yufeng -- Song, Henry -- Bell, Stephanie Nicole -- Davis, Clay -- Johnson, Angela Jolivet -- Lee, Sandra -- Nazareth, Lynne V -- Patel, Bella Mayurkumar -- Pu, Ling-Ling -- Vattathil, Selina -- Williams, Rex Lee Jr -- Curry, Stacey -- Hamilton, Cerissa -- Sodergren, Erica -- Wheeler, David A -- Barris, Wes -- Bennett, Gary L -- Eggen, Andre -- Green, Ronnie D -- Harhay, Gregory P -- Hobbs, Matthew -- Jann, Oliver -- Keele, John W -- Kent, Matthew P -- Lien, Sigbjorn -- McKay, Stephanie D -- McWilliam, Sean -- Ratnakumar, Abhirami -- Schnabel, Robert D -- Smith, Timothy -- Snelling, Warren M -- Sonstegard, Tad S -- Stone, Roger T -- Sugimoto, Yoshikazu -- Takasuga, Akiko -- Taylor, Jeremy F -- Van Tassell, Curtis P -- Macneil, Michael D -- Abatepaulo, Antonio R R -- Abbey, Colette A -- Ahola, Virpi -- Almeida, Iassudara G -- Amadio, Ariel F -- Anatriello, Elen -- Bahadue, Suria M -- Biase, Fernando H -- Boldt, Clayton R -- Carroll, Jeffery A -- Carvalho, Wanessa A -- Cervelatti, Eliane P -- Chacko, Elsa -- Chapin, Jennifer E -- Cheng, Ye -- Choi, Jungwoo -- Colley, Adam J -- de Campos, Tatiana A -- De Donato, Marcos -- Santos, Isabel K F de Miranda -- de Oliveira, Carlo J F -- Deobald, Heather -- Devinoy, Eve -- Donohue, Kaitlin E -- Dovc, Peter -- Eberlein, Annett -- Fitzsimmons, Carolyn J -- Franzin, Alessandra M -- Garcia, Gustavo R -- Genini, Sem -- Gladney, Cody J -- Grant, Jason R -- Greaser, Marion L -- Green, Jonathan A -- Hadsell, Darryl L -- Hakimov, Hatam A -- Halgren, Rob -- Harrow, Jennifer L -- Hart, Elizabeth A -- Hastings, Nicola -- Hernandez, Marta -- Hu, Zhi-Liang -- Ingham, Aaron -- Iso-Touru, Terhi -- Jamis, Catherine -- Jensen, Kirsty -- Kapetis, Dimos -- Kerr, Tovah -- Khalil, Sari S -- Khatib, Hasan -- Kolbehdari, Davood -- Kumar, Charu G -- Kumar, Dinesh -- Leach, Richard -- Lee, Justin C-M -- Li, Changxi -- Logan, Krystin M -- Malinverni, Roberto -- Marques, Elisa -- Martin, William F -- Martins, Natalia F -- Maruyama, Sandra R -- Mazza, Raffaele -- McLean, Kim L -- Medrano, Juan F -- Moreno, Barbara T -- More, Daniela D -- Muntean, Carl T -- Nandakumar, Hari P -- Nogueira, Marcelo F G -- Olsaker, Ingrid -- Pant, Sameer D -- Panzitta, Francesca -- Pastor, Rosemeire C P -- Poli, Mario A -- Poslusny, Nathan -- Rachagani, Satyanarayana -- Ranganathan, Shoba -- Razpet, Andrej -- Riggs, Penny K -- Rincon, Gonzalo -- Rodriguez-Osorio, Nelida -- Rodriguez-Zas, Sandra L -- Romero, Natasha E -- Rosenwald, Anne -- Sando, Lillian -- Schmutz, Sheila M -- Shen, Libing -- Sherman, Laura -- Southey, Bruce R -- Lutzow, Ylva Strandberg -- Sweedler, Jonathan V -- Tammen, Imke -- Telugu, Bhanu Prakash V L -- Urbanski, Jennifer M -- Utsunomiya, Yuri T -- Verschoor, Chris P -- Waardenberg, Ashley J -- Wang, Zhiquan -- Ward, Robert -- Weikard, Rosemarie -- Welsh, Thomas H Jr -- White, Stephen N -- Wilming, Laurens G -- Wunderlich, Kris R -- Yang, Jianqi -- Zhao, Feng-Qi -- 062023/Wellcome Trust/United Kingdom -- 077198/Wellcome Trust/United Kingdom -- BBS/B/13438/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBS/B/13446/Biotechnology and Biological Sciences Research Council/United Kingdom -- P30 DA018310/DA/NIDA NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- U54 HG003273-04/HG/NHGRI NIH HHS/ -- U54 HG003273-04S1/HG/NHGRI NIH HHS/ -- U54 HG003273-05/HG/NHGRI NIH HHS/ -- U54 HG003273-05S1/HG/NHGRI NIH HHS/ -- U54 HG003273-05S2/HG/NHGRI NIH HHS/ -- U54 HG003273-06/HG/NHGRI NIH HHS/ -- U54 HG003273-06S1/HG/NHGRI NIH HHS/ -- U54 HG003273-06S2/HG/NHGRI NIH HHS/ -- U54 HG003273-07/HG/NHGRI NIH HHS/ -- U54 HG003273-08/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2009 Apr 24;324(5926):522-8. doi: 10.1126/science.1169588.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19390049" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Animals ; Animals, Domestic ; *Biological Evolution ; Cattle ; Evolution, Molecular ; Female ; Genetic Variation ; *Genome ; Humans ; Male ; MicroRNAs/genetics ; Molecular Sequence Data ; Proteins/genetics ; Sequence Analysis, DNA ; Species Specificity ; Synteny
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Adaptive evolution of pelvic reduction in sticklebacks by recurrent deletion of a Pitx1 enhancer (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-17
    Description: The molecular mechanisms underlying major phenotypic changes that have evolved repeatedly in nature are generally unknown. Pelvic loss in different natural populations of threespine stickleback fish has occurred through regulatory mutations deleting a tissue-specific enhancer of the Pituitary homeobox transcription factor 1 (Pitx1) gene. The high prevalence of deletion mutations at Pitx1 may be influenced by inherent structural features of the locus. Although Pitx1 null mutations are lethal in laboratory animals, Pitx1 regulatory mutations show molecular signatures of positive selection in pelvic-reduced populations. These studies illustrate how major expression and morphological changes can arise from single mutational leaps in natural populations, producing new adaptive alleles via recurrent regulatory alterations in a key developmental control gene.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3109066/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3109066/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chan, Yingguang Frank -- Marks, Melissa E -- Jones, Felicity C -- Villarreal, Guadalupe Jr -- Shapiro, Michael D -- Brady, Shannon D -- Southwick, Audrey M -- Absher, Devin M -- Grimwood, Jane -- Schmutz, Jeremy -- Myers, Richard M -- Petrov, Dmitri -- Jonsson, Bjarni -- Schluter, Dolph -- Bell, Michael A -- Kingsley, David M -- P50 HG002568/HG/NHGRI NIH HHS/ -- P50 HG002568-09/HG/NHGRI NIH HHS/ -- P50 HG02568/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jan 15;327(5963):302-5. doi: 10.1126/science.1182213. Epub 2009 Dec 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology and Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007865" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; *Biological Evolution ; Chromosome Fragile Sites ; Chromosome Mapping ; Crosses, Genetic ; DNA, Intergenic ; *Enhancer Elements, Genetic ; Fish Proteins/*genetics ; Molecular Sequence Data ; Mutation ; Paired Box Transcription Factors/*genetics ; Pelvis/anatomy & histology ; Selection, Genetic ; *Sequence Deletion ; Smegmamorpha/*anatomy & histology/*genetics/growth & development
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    The Chlamydomonas genome reveals the evolution of key animal and plant functions (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-10-13
    Description: Chlamydomonas reinhardtii is a unicellular green alga whose lineage diverged from land plants over 1 billion years ago. It is a model system for studying chloroplast-based photosynthesis, as well as the structure, assembly, and function of eukaryotic flagella (cilia), which were inherited from the common ancestor of plants and animals, but lost in land plants. We sequenced the approximately 120-megabase nuclear genome of Chlamydomonas and performed comparative phylogenomic analyses, identifying genes encoding uncharacterized proteins that are likely associated with the function and biogenesis of chloroplasts or eukaryotic flagella. Analyses of the Chlamydomonas genome advance our understanding of the ancestral eukaryotic cell, reveal previously unknown genes associated with photosynthetic and flagellar functions, and establish links between ciliopathy and the composition and function of flagella.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2875087/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2875087/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Merchant, Sabeeha S -- Prochnik, Simon E -- Vallon, Olivier -- Harris, Elizabeth H -- Karpowicz, Steven J -- Witman, George B -- Terry, Astrid -- Salamov, Asaf -- Fritz-Laylin, Lillian K -- Marechal-Drouard, Laurence -- Marshall, Wallace F -- Qu, Liang-Hu -- Nelson, David R -- Sanderfoot, Anton A -- Spalding, Martin H -- Kapitonov, Vladimir V -- Ren, Qinghu -- Ferris, Patrick -- Lindquist, Erika -- Shapiro, Harris -- Lucas, Susan M -- Grimwood, Jane -- Schmutz, Jeremy -- Cardol, Pierre -- Cerutti, Heriberto -- Chanfreau, Guillaume -- Chen, Chun-Long -- Cognat, Valerie -- Croft, Martin T -- Dent, Rachel -- Dutcher, Susan -- Fernandez, Emilio -- Fukuzawa, Hideya -- Gonzalez-Ballester, David -- Gonzalez-Halphen, Diego -- Hallmann, Armin -- Hanikenne, Marc -- Hippler, Michael -- Inwood, William -- Jabbari, Kamel -- Kalanon, Ming -- Kuras, Richard -- Lefebvre, Paul A -- Lemaire, Stephane D -- Lobanov, Alexey V -- Lohr, Martin -- Manuell, Andrea -- Meier, Iris -- Mets, Laurens -- Mittag, Maria -- Mittelmeier, Telsa -- Moroney, James V -- Moseley, Jeffrey -- Napoli, Carolyn -- Nedelcu, Aurora M -- Niyogi, Krishna -- Novoselov, Sergey V -- Paulsen, Ian T -- Pazour, Greg -- Purton, Saul -- Ral, Jean-Philippe -- Riano-Pachon, Diego Mauricio -- Riekhof, Wayne -- Rymarquis, Linda -- Schroda, Michael -- Stern, David -- Umen, James -- Willows, Robert -- Wilson, Nedra -- Zimmer, Sara Lana -- Allmer, Jens -- Balk, Janneke -- Bisova, Katerina -- Chen, Chong-Jian -- Elias, Marek -- Gendler, Karla -- Hauser, Charles -- Lamb, Mary Rose -- Ledford, Heidi -- Long, Joanne C -- Minagawa, Jun -- Page, M Dudley -- Pan, Junmin -- Pootakham, Wirulda -- Roje, Sanja -- Rose, Annkatrin -- Stahlberg, Eric -- Terauchi, Aimee M -- Yang, Pinfen -- Ball, Steven -- Bowler, Chris -- Dieckmann, Carol L -- Gladyshev, Vadim N -- Green, Pamela -- Jorgensen, Richard -- Mayfield, Stephen -- Mueller-Roeber, Bernd -- Rajamani, Sathish -- Sayre, Richard T -- Brokstein, Peter -- Dubchak, Inna -- Goodstein, David -- Hornick, Leila -- Huang, Y Wayne -- Jhaveri, Jinal -- Luo, Yigong -- Martinez, Diego -- Ngau, Wing Chi Abby -- Otillar, Bobby -- Poliakov, Alexander -- Porter, Aaron -- Szajkowski, Lukasz -- Werner, Gregory -- Zhou, Kemin -- Grigoriev, Igor V -- Rokhsar, Daniel S -- Grossman, Arthur R -- GM07185/GM/NIGMS NIH HHS/ -- GM42143/GM/NIGMS NIH HHS/ -- R01 GM032843/GM/NIGMS NIH HHS/ -- R01 GM042143/GM/NIGMS NIH HHS/ -- R01 GM042143-09/GM/NIGMS NIH HHS/ -- R01 GM060992/GM/NIGMS NIH HHS/ -- R01 GM062915-06/GM/NIGMS NIH HHS/ -- R37 GM030626/GM/NIGMS NIH HHS/ -- R37 GM042143/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Oct 12;318(5848):245-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, University of California at Los Angeles, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17932292" target="_blank"〉PubMed〈/a〉
    Keywords: Algal Proteins/*genetics/*physiology ; Animals ; *Biological Evolution ; Chlamydomonas reinhardtii/*genetics/physiology ; Chloroplasts/metabolism ; Computational Biology ; DNA, Algal/genetics ; Flagella/metabolism ; Genes ; *Genome ; Genomics ; Membrane Transport Proteins/genetics/physiology ; Molecular Sequence Data ; Multigene Family ; Photosynthesis/genetics ; Phylogeny ; Plants/genetics ; Proteome ; Sequence Analysis, DNA
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    The genome of the African trypanosome Trypanosoma brucei (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-07-16
    Description: African trypanosomes cause human sleeping sickness and livestock trypanosomiasis in sub-Saharan Africa. We present the sequence and analysis of the 11 megabase-sized chromosomes of Trypanosoma brucei. The 26-megabase genome contains 9068 predicted genes, including approximately 900 pseudogenes and approximately 1700 T. brucei-specific genes. Large subtelomeric arrays contain an archive of 806 variant surface glycoprotein (VSG) genes used by the parasite to evade the mammalian immune system. Most VSG genes are pseudogenes, which may be used to generate expressed mosaic genes by ectopic recombination. Comparisons of the cytoskeleton and endocytic trafficking systems with those of humans and other eukaryotic organisms reveal major differences. A comparison of metabolic pathways encoded by the genomes of T. brucei, T. cruzi, and Leishmania major reveals the least overall metabolic capability in T. brucei and the greatest in L. major. Horizontal transfer of genes of bacterial origin has contributed to some of the metabolic differences in these parasites, and a number of novel potential drug targets have been identified.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berriman, Matthew -- Ghedin, Elodie -- Hertz-Fowler, Christiane -- Blandin, Gaelle -- Renauld, Hubert -- Bartholomeu, Daniella C -- Lennard, Nicola J -- Caler, Elisabet -- Hamlin, Nancy E -- Haas, Brian -- Bohme, Ulrike -- Hannick, Linda -- Aslett, Martin A -- Shallom, Joshua -- Marcello, Lucio -- Hou, Lihua -- Wickstead, Bill -- Alsmark, U Cecilia M -- Arrowsmith, Claire -- Atkin, Rebecca J -- Barron, Andrew J -- Bringaud, Frederic -- Brooks, Karen -- Carrington, Mark -- Cherevach, Inna -- Chillingworth, Tracey-Jane -- Churcher, Carol -- Clark, Louise N -- Corton, Craig H -- Cronin, Ann -- Davies, Rob M -- Doggett, Jonathon -- Djikeng, Appolinaire -- Feldblyum, Tamara -- Field, Mark C -- Fraser, Audrey -- Goodhead, Ian -- Hance, Zahra -- Harper, David -- Harris, Barbara R -- Hauser, Heidi -- Hostetler, Jessica -- Ivens, Al -- Jagels, Kay -- Johnson, David -- Johnson, Justin -- Jones, Kristine -- Kerhornou, Arnaud X -- Koo, Hean -- Larke, Natasha -- Landfear, Scott -- Larkin, Christopher -- Leech, Vanessa -- Line, Alexandra -- Lord, Angela -- Macleod, Annette -- Mooney, Paul J -- Moule, Sharon -- Martin, David M A -- Morgan, Gareth W -- Mungall, Karen -- Norbertczak, Halina -- Ormond, Doug -- Pai, Grace -- Peacock, Chris S -- Peterson, Jeremy -- Quail, Michael A -- Rabbinowitsch, Ester -- Rajandream, Marie-Adele -- Reitter, Chris -- Salzberg, Steven L -- Sanders, Mandy -- Schobel, Seth -- Sharp, Sarah -- Simmonds, Mark -- Simpson, Anjana J -- Tallon, Luke -- Turner, C Michael R -- Tait, Andrew -- Tivey, Adrian R -- Van Aken, Susan -- Walker, Danielle -- Wanless, David -- Wang, Shiliang -- White, Brian -- White, Owen -- Whitehead, Sally -- Woodward, John -- Wortman, Jennifer -- Adams, Mark D -- Embley, T Martin -- Gull, Keith -- Ullu, Elisabetta -- Barry, J David -- Fairlamb, Alan H -- Opperdoes, Fred -- Barrell, Barclay G -- Donelson, John E -- Hall, Neil -- Fraser, Claire M -- Melville, Sara E -- El-Sayed, Najib M -- AI43062/AI/NIAID NIH HHS/ -- R01 AI043062/AI/NIAID NIH HHS/ -- U01 AI043062/AI/NIAID NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2005 Jul 15;309(5733):416-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton CB10 1SA, UK. mb4@sanger.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16020726" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/metabolism ; Animals ; Antigenic Variation ; Antigens, Protozoan/chemistry/genetics/immunology ; Carbohydrate Metabolism ; Chromosomes/genetics ; Cytoskeleton/chemistry/genetics/physiology ; Ergosterol/biosynthesis ; Genes, Protozoan ; *Genome, Protozoan ; Glutathione/*analogs & derivatives/metabolism ; Glycosylphosphatidylinositols/biosynthesis ; Humans ; Lipid Metabolism ; Molecular Sequence Data ; Protein Transport ; Protozoan Proteins/chemistry/*genetics/metabolism ; Pseudogenes ; Purines/metabolism ; Pyrimidines/biosynthesis ; Recombination, Genetic ; *Sequence Analysis, DNA ; Spermidine/*analogs & derivatives/metabolism ; Trypanosoma brucei brucei/chemistry/*genetics/immunology/metabolism ; Trypanosomiasis, African/parasitology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    The CRAC channel consists of a tetramer formed by Stim-induced dimerization of Orai dimers (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-09-30
    Description: Ca(2+)-release-activated Ca(2+) (CRAC) channels underlie sustained Ca(2+) signalling in lymphocytes and numerous other cells after Ca(2+) liberation from the endoplasmic reticulum (ER). RNA interference screening approaches identified two proteins, Stim and Orai, that together form the molecular basis for CRAC channel activity. Stim senses depletion of the ER Ca(2+) store and physically relays this information by translocating from the ER to junctions adjacent to the plasma membrane, and Orai embodies the pore of the plasma membrane calcium channel. A close interaction between Stim and Orai, identified by co-immunoprecipitation and by Forster resonance energy transfer, is involved in the opening of the Ca(2+) channel formed by Orai subunits. Most ion channels are multimers of pore-forming subunits surrounding a central channel, which are preassembled in the ER and transported in their final stoichiometry to the plasma membrane. Here we show, by biochemical analysis after cross-linking in cell lysates and intact cells and by using non-denaturing gel electrophoresis without cross-linking, that Orai is predominantly a dimer in the plasma membrane under resting conditions. Moreover, single-molecule imaging of green fluorescent protein (GFP)-tagged Orai expressed in Xenopus oocytes showed predominantly two-step photobleaching, again consistent with a dimeric basal state. In contrast, co-expression of GFP-tagged Orai with the carboxy terminus of Stim as a cytosolic protein to activate the Orai channel without inducing Ca(2+) store depletion or clustering of Orai into punctae yielded mostly four-step photobleaching, consistent with a tetrameric stoichiometry of the active Orai channel. Interaction with the C terminus of Stim thus induces Orai dimers to dimerize, forming tetramers that constitute the Ca(2+)-selective pore. This represents a new mechanism in which assembly and activation of the functional ion channel are mediated by the same triggering molecule.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2597643/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2597643/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Penna, Aubin -- Demuro, Angelo -- Yeromin, Andriy V -- Zhang, Shenyuan L -- Safrina, Olga -- Parker, Ian -- Cahalan, Michael D -- P30 CA062203/CA/NCI NIH HHS/ -- R37 NS014609/NS/NINDS NIH HHS/ -- R37 NS014609-29/NS/NINDS NIH HHS/ -- England -- Nature. 2008 Nov 6;456(7218):116-20. doi: 10.1038/nature07338. Epub 2008 Sep 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Biophysics, University of California Irvine, California 92697-4561, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18820677" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium Channels/*chemistry/genetics/*metabolism ; Cell Line ; Cross-Linking Reagents ; Drosophila Proteins/*chemistry/genetics/*metabolism ; Drosophila melanogaster/*chemistry/*metabolism ; Humans ; Membrane Proteins/*chemistry/genetics/*metabolism ; Oocytes/metabolism ; Photobleaching ; Protein Multimerization ; Protein Structure, Quaternary ; Xenopus ; Xenopus Proteins/*chemistry/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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    The M2 splice isoform of pyruvate kinase is important for cancer metabolism and tumour growth (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-03-14
    Description: Many tumour cells have elevated rates of glucose uptake but reduced rates of oxidative phosphorylation. This persistence of high lactate production by tumours in the presence of oxygen, known as aerobic glycolysis, was first noted by Otto Warburg more than 75 yr ago. How tumour cells establish this altered metabolic phenotype and whether it is essential for tumorigenesis is as yet unknown. Here we show that a single switch in a splice isoform of the glycolytic enzyme pyruvate kinase is necessary for the shift in cellular metabolism to aerobic glycolysis and that this promotes tumorigenesis. Tumour cells have been shown to express exclusively the embryonic M2 isoform of pyruvate kinase. Here we use short hairpin RNA to knockdown pyruvate kinase M2 expression in human cancer cell lines and replace it with pyruvate kinase M1. Switching pyruvate kinase expression to the M1 (adult) isoform leads to reversal of the Warburg effect, as judged by reduced lactate production and increased oxygen consumption, and this correlates with a reduced ability to form tumours in nude mouse xenografts. These results demonstrate that M2 expression is necessary for aerobic glycolysis and that this metabolic phenotype provides a selective growth advantage for tumour cells in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Christofk, Heather R -- Vander Heiden, Matthew G -- Harris, Marian H -- Ramanathan, Arvind -- Gerszten, Robert E -- Wei, Ru -- Fleming, Mark D -- Schreiber, Stuart L -- Cantley, Lewis C -- R01 GM056203/GM/NIGMS NIH HHS/ -- T32 CA009172/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2008 Mar 13;452(7184):230-3. doi: 10.1038/nature06734.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Systems Biology, Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18337823" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing/*genetics ; Animals ; Cell Line, Tumor ; Cell Proliferation ; Fructosediphosphates/metabolism ; Gene Expression Regulation, Neoplastic ; Glycolysis ; Humans ; Lactic Acid/metabolism ; Lung Neoplasms/genetics/metabolism/pathology ; Male ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Neoplasms/enzymology/genetics/*metabolism/*pathology ; Oxidative Phosphorylation ; Oxygen Consumption ; Pyruvate Kinase/*genetics/*metabolism ; Pyruvic Acid/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Regulation of progenitor cell proliferation and granulocyte function by microRNA-223 (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-02-19
    Description: MicroRNAs are abundant in animal genomes and have been predicted to have important roles in a broad range of gene expression programmes. Despite this prominence, there is a dearth of functional knowledge regarding individual mammalian microRNAs. Using a loss-of-function allele in mice, we report here that the myeloid-specific microRNA-223 (miR-223) negatively regulates progenitor proliferation and granulocyte differentiation and activation. miR-223 (also called Mirn223) mutant mice have an expanded granulocytic compartment resulting from a cell-autonomous increase in the number of granulocyte progenitors. We show that Mef2c, a transcription factor that promotes myeloid progenitor proliferation, is a target of miR-223, and that genetic ablation of Mef2c suppresses progenitor expansion and corrects the neutrophilic phenotype in miR-223 null mice. In addition, granulocytes lacking miR-223 are hypermature, hypersensitive to activating stimuli and display increased fungicidal activity. As a consequence of this neutrophil hyperactivity, miR-223 mutant mice spontaneously develop inflammatory lung pathology and exhibit exaggerated tissue destruction after endotoxin challenge. Our data support a model in which miR-223 acts as a fine-tuner of granulocyte production and the inflammatory response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Johnnidis, Jonathan B -- Harris, Marian H -- Wheeler, Robert T -- Stehling-Sun, Sandra -- Lam, Michael H -- Kirak, Oktay -- Brummelkamp, Thijn R -- Fleming, Mark D -- Camargo, Fernando D -- England -- Nature. 2008 Feb 28;451(7182):1125-9. doi: 10.1038/nature06607. Epub 2008 Feb 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18278031" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Cell Differentiation ; *Cell Proliferation ; Gene Deletion ; Granulocytes/*cytology/immunology/pathology/*physiology ; Inflammation/genetics/immunology/pathology ; Lung/pathology ; MEF2 Transcription Factors ; Mice ; Mice, Knockout ; MicroRNAs/*genetics/*metabolism ; Myogenic Regulatory Factors/genetics/metabolism ; Neutrophils/physiology ; Phenotype ; Stem Cells/*cytology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Haem homeostasis is regulated by the conserved and concerted functions of HRG-1 proteins (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-04-18
    Description: Haems are metalloporphyrins that serve as prosthetic groups for various biological processes including respiration, gas sensing, xenobiotic detoxification, cell differentiation, circadian clock control, metabolic reprogramming and microRNA processing. With a few exceptions, haem is synthesized by a multistep biosynthetic pathway comprising defined intermediates that are highly conserved throughout evolution. Despite our extensive knowledge of haem biosynthesis and degradation, the cellular pathways and molecules that mediate intracellular haem trafficking are unknown. The experimental setback in identifying haem trafficking pathways has been the inability to dissociate the highly regulated cellular synthesis and degradation of haem from intracellular trafficking events. Caenorhabditis elegans and related helminths are natural haem auxotrophs that acquire environmental haem for incorporation into haemoproteins, which have vertebrate orthologues. Here we show, by exploiting this auxotrophy to identify HRG-1 proteins in C. elegans, that these proteins are essential for haem homeostasis and normal development in worms and vertebrates. Depletion of hrg-1, or its paralogue hrg-4, in worms results in the disruption of organismal haem sensing and an abnormal response to haem analogues. HRG-1 and HRG-4 are previously unknown transmembrane proteins, which reside in distinct intracellular compartments. Transient knockdown of hrg-1 in zebrafish leads to hydrocephalus, yolk tube malformations and, most strikingly, profound defects in erythropoiesis-phenotypes that are fully rescued by worm HRG-1. Human and worm proteins localize together, and bind and transport haem, thus establishing an evolutionarily conserved function for HRG-1. These findings reveal conserved pathways for cellular haem trafficking in animals that define the model for eukaryotic haem transport. Thus, uncovering the mechanisms of haem transport in C. elegans may provide insights into human disorders of haem metabolism and reveal new drug targets for developing anthelminthics to combat worm infestations.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4058867/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4058867/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rajagopal, Abbhirami -- Rao, Anita U -- Amigo, Julio -- Tian, Meng -- Upadhyay, Sanjeev K -- Hall, Caitlin -- Uhm, Suji -- Mathew, M K -- Fleming, Mark D -- Paw, Barry H -- Krause, Michael -- Hamza, Iqbal -- R01 DK074797/DK/NIDDK NIH HHS/ -- R01 DK074797-01/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- Intramural NIH HHS/ -- England -- Nature. 2008 Jun 19;453(7198):1127-31. doi: 10.1038/nature06934. Epub 2008 Apr 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Animal & Avian Sciences, University of Maryland, College Park, Maryland 20742, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18418376" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport/drug effects ; Caenorhabditis elegans/genetics/*metabolism ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Cell Line ; Erythropoiesis ; Heme/*metabolism/pharmacology ; Hemeproteins/genetics/*metabolism ; *Homeostasis ; Humans ; Metalloporphyrins/metabolism ; Zebrafish/embryology/genetics/*metabolism ; Zebrafish Proteins/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Sequencing the nuclear genome of the extinct woolly mammoth (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-11-21
    Description: In 1994, two independent groups extracted DNA from several Pleistocene epoch mammoths and noted differences among individual specimens. Subsequently, DNA sequences have been published for a number of extinct species. However, such ancient DNA is often fragmented and damaged, and studies to date have typically focused on short mitochondrial sequences, never yielding more than a fraction of a per cent of any nuclear genome. Here we describe 4.17 billion bases (Gb) of sequence from several mammoth specimens, 3.3 billion (80%) of which are from the woolly mammoth (Mammuthus primigenius) genome and thus comprise an extensive set of genome-wide sequence from an extinct species. Our data support earlier reports that elephantid genomes exceed 4 Gb. The estimated divergence rate between mammoth and African elephant is half of that between human and chimpanzee. The observed number of nucleotide differences between two particular mammoths was approximately one-eighth of that between one of them and the African elephant, corresponding to a separation between the mammoths of 1.5-2.0 Myr. The estimated probability that orthologous elephant and mammoth amino acids differ is 0.002, corresponding to about one residue per protein. Differences were discovered between mammoth and African elephant in amino-acid positions that are otherwise invariant over several billion years of combined mammalian evolution. This study shows that nuclear genome sequencing of extinct species can reveal population differences not evident from the fossil record, and perhaps even discover genetic factors that affect extinction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Webb -- Drautz, Daniela I -- Ratan, Aakrosh -- Pusey, Barbara -- Qi, Ji -- Lesk, Arthur M -- Tomsho, Lynn P -- Packard, Michael D -- Zhao, Fangqing -- Sher, Andrei -- Tikhonov, Alexei -- Raney, Brian -- Patterson, Nick -- Lindblad-Toh, Kerstin -- Lander, Eric S -- Knight, James R -- Irzyk, Gerard P -- Fredrikson, Karin M -- Harkins, Timothy T -- Sheridan, Sharon -- Pringle, Tom -- Schuster, Stephan C -- HG002238/HG/NHGRI NIH HHS/ -- England -- Nature. 2008 Nov 20;456(7220):387-90. doi: 10.1038/nature07446.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Pennsylvania State University, Center for Comparative Genomics and Bioinformatics, 310 Wartik Building, University Park, Pennsylvania 16802, USA. webb@bx.psu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19020620" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Animals ; Cell Nucleus/*genetics ; Conserved Sequence/genetics ; Elephants/anatomy & histology/*genetics ; *Evolution, Molecular ; *Extinction, Biological ; Female ; *Fossils ; Genome/*genetics ; *Genomics ; Hair/metabolism ; Humans ; India ; Male ; Phylogeny ; Sequence Analysis, DNA/*methods
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Agrochemicals increase trematode infections in a declining amphibian species (2008)
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    Publication Date: 2008-10-31
    Description: Global amphibian declines have often been attributed to disease, but ignorance of the relative importance and mode of action of potential drivers of infection has made it difficult to develop effective remediation. In a field study, here we show that the widely used herbicide, atrazine, was the best predictor (out of more than 240 plausible candidates) of the abundance of larval trematodes (parasitic flatworms) in the declining northern leopard frog Rana pipiens. The effects of atrazine were consistent across trematode taxa. The combination of atrazine and phosphate--principal agrochemicals in global corn and sorghum production--accounted for 74% of the variation in the abundance of these often debilitating larval trematodes (atrazine alone accounted for 51%). Analysis of field data supported a causal mechanism whereby both agrochemicals increase exposure and susceptibility to larval trematodes by augmenting snail intermediate hosts and suppressing amphibian immunity. A mesocosm experiment demonstrated that, relative to control tanks, atrazine tanks had immunosuppressed tadpoles, had significantly more attached algae and snails, and had tadpoles with elevated trematode loads, further supporting a causal relationship between atrazine and elevated trematode infections in amphibians. These results raise concerns about the role of atrazine and phosphate in amphibian declines, and illustrate the value of quantifying the relative importance of several possible drivers of disease risk while determining the mechanisms by which they facilitate disease emergence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rohr, Jason R -- Schotthoefer, Anna M -- Raffel, Thomas R -- Carrick, Hunter J -- Halstead, Neal -- Hoverman, Jason T -- Johnson, Catherine M -- Johnson, Lucinda B -- Lieske, Camilla -- Piwoni, Marvin D -- Schoff, Patrick K -- Beasley, Val R -- England -- Nature. 2008 Oct 30;455(7217):1235-9. doi: 10.1038/nature07281.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biology Department, University of South Florida, Tampa, Florida 33620, USA. jasonrohr@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18972018" target="_blank"〉PubMed〈/a〉
    Keywords: Agrochemicals/*pharmacology ; Animals ; Atrazine/pharmacology ; Biodiversity ; Disease Susceptibility/chemically induced/*veterinary ; Herbicides/pharmacology ; Larva/drug effects/physiology ; Phosphates/pharmacology ; Population Density ; Rana pipiens/immunology/*parasitology/*physiology ; Trematoda/*drug effects/growth & development/*physiology ; Trematode Infections/chemically induced/parasitology/*veterinary ; Wetlands
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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