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  • 1
    Publication Date: 2005-07-16
    Description: Leishmania species cause a spectrum of human diseases in tropical and subtropical regions of the world. We have sequenced the 36 chromosomes of the 32.8-megabase haploid genome of Leishmania major (Friedlin strain) and predict 911 RNA genes, 39 pseudogenes, and 8272 protein-coding genes, of which 36% can be ascribed a putative function. These include genes involved in host-pathogen interactions, such as proteolytic enzymes, and extensive machinery for synthesis of complex surface glycoconjugates. The organization of protein-coding genes into long, strand-specific, polycistronic clusters and lack of general transcription factors in the L. major, Trypanosoma brucei, and Trypanosoma cruzi (Tritryp) genomes suggest that the mechanisms regulating RNA polymerase II-directed transcription are distinct from those operating in other eukaryotes, although the trypanosomatids appear capable of chromatin remodeling. Abundant RNA-binding proteins are encoded in the Tritryp genomes, consistent with active posttranscriptional regulation of gene expression.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1470643/" 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/PMC1470643/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ivens, Alasdair C -- Peacock, Christopher S -- Worthey, Elizabeth A -- Murphy, Lee -- Aggarwal, Gautam -- Berriman, Matthew -- Sisk, Ellen -- Rajandream, Marie-Adele -- Adlem, Ellen -- Aert, Rita -- Anupama, Atashi -- Apostolou, Zina -- Attipoe, Philip -- Bason, Nathalie -- Bauser, Christopher -- Beck, Alfred -- Beverley, Stephen M -- Bianchettin, Gabriella -- Borzym, Katja -- Bothe, Gordana -- Bruschi, Carlo V -- Collins, Matt -- Cadag, Eithon -- Ciarloni, Laura -- Clayton, Christine -- Coulson, Richard M R -- Cronin, Ann -- Cruz, Angela K -- Davies, Robert M -- De Gaudenzi, Javier -- Dobson, Deborah E -- Duesterhoeft, Andreas -- Fazelina, Gholam -- Fosker, Nigel -- Frasch, Alberto Carlos -- Fraser, Audrey -- Fuchs, Monika -- Gabel, Claudia -- Goble, Arlette -- Goffeau, Andre -- Harris, David -- Hertz-Fowler, Christiane -- Hilbert, Helmut -- Horn, David -- Huang, Yiting -- Klages, Sven -- Knights, Andrew -- Kube, Michael -- Larke, Natasha -- Litvin, Lyudmila -- Lord, Angela -- Louie, Tin -- Marra, Marco -- Masuy, David -- Matthews, Keith -- Michaeli, Shulamit -- Mottram, Jeremy C -- Muller-Auer, Silke -- Munden, Heather -- Nelson, Siri -- Norbertczak, Halina -- Oliver, Karen -- O'neil, Susan -- Pentony, Martin -- Pohl, Thomas M -- Price, Claire -- Purnelle, Benedicte -- Quail, Michael A -- Rabbinowitsch, Ester -- Reinhardt, Richard -- Rieger, Michael -- Rinta, Joel -- Robben, Johan -- Robertson, Laura -- Ruiz, Jeronimo C -- Rutter, Simon -- Saunders, David -- Schafer, Melanie -- Schein, Jacquie -- Schwartz, David C -- Seeger, Kathy -- Seyler, Amber -- Sharp, Sarah -- Shin, Heesun -- Sivam, Dhileep -- Squares, Rob -- Squares, Steve -- Tosato, Valentina -- Vogt, Christy -- Volckaert, Guido -- Wambutt, Rolf -- Warren, Tim -- Wedler, Holger -- Woodward, John -- Zhou, Shiguo -- Zimmermann, Wolfgang -- Smith, Deborah F -- Blackwell, Jenefer M -- Stuart, Kenneth D -- Barrell, Bart -- Myler, Peter J -- R01 AI040599/AI/NIAID NIH HHS/ -- R01 AI053667/AI/NIAID NIH HHS/ -- U01 AI040599/AI/NIAID NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2005 Jul 15;309(5733):436-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire CB10 1SA, UK. alicat@sanger.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16020728" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromatin/genetics/metabolism ; Gene Expression Regulation ; Genes, Protozoan ; Genes, rRNA ; *Genome, Protozoan ; Glycoconjugates/biosynthesis/metabolism ; Leishmania major/chemistry/*genetics/metabolism ; Leishmaniasis, Cutaneous/parasitology ; Lipid Metabolism ; Membrane Proteins/biosynthesis/chemistry/genetics/metabolism ; Molecular Sequence Data ; Multigene Family ; Protein Biosynthesis ; Protein Processing, Post-Translational ; Protozoan Proteins/biosynthesis/chemistry/genetics/metabolism ; RNA Processing, Post-Transcriptional ; RNA Splicing ; RNA, Protozoan/genetics/metabolism ; *Sequence Analysis, DNA ; Transcription, Genetic
    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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  • 2
    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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  • 3
  • 4
    Publication Date: 2006-11-23
    Print ISSN: 1466-4879
    Electronic ISSN: 1476-5470
    Topics: Biology , Medicine
    Published by Springer Nature
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  • 8
    Publication Date: 1997-09-29
    Description: In the 1970s and 1980s, analysis of recombinant inbred, congenic and recombinant haplotype mouse strains permitted us to effectively ‘scan’ the murine genome for genes controlling resistance and susceptibility to leishmanial infections. Five major regions of the genome were implicated in the control of infections caused by different Leishmania species which, because they show conserved synteny with regions of the human genome, immediately provides candidate gene regions for human disease susceptibility genes. A common intramacrophage niche for leishmanial and mycobacterial pathogens, and a similar spectrum of immune response and disease phenotypes, also led to the prediction that the same genes/candidate gene regions might be responsible for genetic susceptibility to mycobacterial infections such as leprosy and tuberculosis. Indeed, one of the murine genes ( Nramp1 ) was identified for its role in controlling a range of intramacrophage pathogens including leishmania, salmonella and mycobacterium infections. In recent studies, multicase family data on visceral leishmaniasis and the mycobacterial diseases, tuberculosis and leprosy, have been collected from north–eastern Brazil and analysed to determine the role of these candidate genes/regions in determining disease susceptibility. Complex segregation analysis provides evidence for one or two major genes controlling susceptibility to tuberculosis in this population. Family–based linkage analyses (combined segregation and linkage analysis; sib–pair analysis), which have the power to detect linkage between marker loci in candidate gene regions and the putative disease susceptibility genes over 10–;20 centimorgans, and transmission disequilibrium testing, which detects allelic associations over 1 centimorgan ( ca. 1 megabase), have been used to examine the role of four regions in determining disease susceptibility and/or immune response phenotype. Our results demonstrate: (i) the major histocompatibility complex (MHC: H–2 in mouse, HLA in man: mouse chromosome 17/human 6p; candidates class II and class III including TNFalpha/beta genes) shows both linkage to, and allelic association with, leprosy per se , but is only weakly associated with visceral leishmaniasis and shows neither linkage to nor allelic association with tuberculosis; (ii) no evidence for linkage between NRAMP1 , the positionally cloned candidate for the murine macrophage resistance gene Ity/Lsh/Bcg (mouse chromosome 1/human 2q35), and susceptibility to tuberculosis or visceral leishmaniasis could be demonstrated in this Brazilian population; (iii) the region of human chromosome 17q (candidates NOS2A , SCYA2–5 ) homologous with distal mouse chromosome 11, originally identified as carrying the Scl1 gene controlling healing versus nonhealing responses to Leishmania major , is linked to tuberculosis susceptibility; and (iv) the ‘T helper 2’ cytokine gene cluster (proximal murine chromosome 11/human 5q; candidates IL4, IL5, IL9, IRF1, CD14) controlling later phases of murine L. major infection, is not linked to human disease susceptibility for any of the three infections, but shows linkage to and highly significant allelic association with ability to mount an immune response to mycobacterial antigens. These studies demonstrate that the ‘mouse–to–man’ strategy, refined by our knowledge of the human immune response to infection, can lead to the identification of important candidate gene regions in man.
    Print ISSN: 0962-8436
    Electronic ISSN: 1471-2970
    Topics: Biology
    Published by The Royal Society
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