Author Report for: Silva JCNo contact information in database for Silva JC
Carlton JM, Adams JH, Silva JC, Bidwell SL, Lorenzi H, Caler E, Crabtree J, Angiuoli SV, Merino EF and Fraser-Liggett CM <30 more author(s)> Carlton JM, Adams JH, Silva JC, Bidwell SL, Lorenzi H, Caler E, Crabtree J, Angiuoli SV, Merino EF, Amedeo P, Cheng Q, Coulson RM, Crabb BS, Del Portillo HA, Essien K, Feldblyum TV, Fernandez-Becerra C, Gilson PR, Gueye AH, Guo X, Kang'a S, Kooij TW, Korsinczky M, Meyer EV, Nene V, Paulsen I, White O, Ralph SA, Ren Q, Sargeant TJ, Salzberg SL, Stoeckert CJ, Sullivan SA, Yamamoto MM, Hoffman SL, Wortman JR, Gardner MJ, Galinski MR, Barnwell JW, Fraser-Liggett CM (- 30) Ref: Nature, 455:757, 2008 : PubMed ESTHER: Carlton_2008_Nature_455_757 PubMedSearch: Carlton 2008 Nature 455 757 PubMedID: 18843361 Gene_locus related to this paper: plakh-b3lb44, plavi-a5kcq0, plavs-a5k2k6, plavs-a5k3z4, plavs-a5k4s6, plavs-a5k5e4, plavs-a5k7t5, plavs-a5k686, plavs-a5kaa1, plavs-a5kaa3, plavs-a5kas6, plavs-a5kcm2 Abstract The human malaria parasite Plasmodium vivax is responsible for 25-40% of the approximately 515 million annual cases of malaria worldwide. Although seldom fatal, the parasite elicits severe and incapacitating clinical symptoms and often causes relapses months after a primary infection has cleared. Despite its importance as a major human pathogen, P. vivax is little studied because it cannot be propagated continuously in the laboratory except in non-human primates. We sequenced the genome of P. vivax to shed light on its distinctive biological features, and as a means to drive development of new drugs and vaccines. Here we describe the synteny and isochore structure of P. vivax chromosomes, and show that the parasite resembles other malaria parasites in gene content and metabolic potential, but possesses novel gene families and potential alternative invasion pathways not recognized previously. Completion of the P. vivax genome provides the scientific community with a valuable resource that can be used to advance investigation into this neglected species. Title: Genomic islands in the pathogenic filamentous fungus Aspergillus fumigatus Fedorova ND, Khaldi N, Joardar VS, Maiti R, Amedeo P, Anderson MJ, Crabtree J, Silva JC, Badger JH and Nierman WC <29 more author(s)> Fedorova ND, Khaldi N, Joardar VS, Maiti R, Amedeo P, Anderson MJ, Crabtree J, Silva JC, Badger JH, Albarraq A, Angiuoli S, Bussey H, Bowyer P, Cotty PJ, Dyer PS, Egan A, Galens K, Fraser-Liggett CM, Haas BJ, Inman JM, Kent R, Lemieux S, Malavazi I, Orvis J, Roemer T, Ronning CM, Sundaram JP, Sutton G, Turner G, Venter JC, White OR, Whitty BR, Youngman P, Wolfe KH, Goldman GH, Wortman JR, Jiang B, Denning DW, Nierman WC (- 29) Ref: PLoS Genet, 4:e1000046, 2008 : PubMed ESTHER: Fedorova_2008_PLoS.Genet_4_E1000046 PubMedSearch: Fedorova 2008 PLoS.Genet 4 E1000046 PubMedID: 18404212 Gene_locus related to this paper: aspcl-a1c4m6, aspcl-a1c5a7, aspcl-a1c6w3, aspcl-a1c8p7, aspcl-a1c8q9, aspcl-a1c9k4, aspcl-a1c759, aspcl-a1c786, aspcl-a1c823, aspcl-a1c859, aspcl-a1c881, aspcl-a1c994, aspcl-a1cag4, aspcl-a1caj8, aspcl-a1cas0, aspcl-a1cc86, aspcl-a1ccq2, aspcl-a1cfv7, aspcl-a1chj6, aspcl-a1cif4, aspcl-a1ck14, aspcl-a1cke4, aspcl-a1ckq1, aspcl-a1cli1, aspcl-a1cln8, aspcl-a1cm72, aspcl-a1cns2, aspcl-a1cpk9, aspcl-a1cra8, aspcl-a1crr5, aspcl-a1crs9, aspcl-a1cs04, aspcl-a1cs39, aspcl-a1cu39, aspcl-atg15, aspcl-axe1, aspcl-cuti1, aspcl-cuti3, aspcl-dapb, aspcl-dpp4, aspcl-dpp5, aspcl-faeb, aspcl-faec1, aspcl-faec2, aspfc-b0xp50, aspfc-b0xu40, aspfc-b0xzj6, aspfc-b0y2h6, aspfc-b0y962, aspfc-b0yaj6, aspfc-dpp5, aspfu-DPP4, aspfu-faeb1, aspfu-faec, aspfu-ppme1, aspfu-q4w9r3, aspfu-q4w9t5, aspfu-q4w9z4, aspfu-q4wa57, aspfu-q4wa78, aspfu-q4wag0, aspfu-q4wal3, aspfu-q4wbc5, aspfu-q4wbj7, aspfu-q4wdg2, aspfu-q4wf06, aspfu-q4wf29, aspfu-q4wf56, aspfu-q4wfq9, aspfu-q4wg73, aspfu-q4wgm4, aspfu-q4win2, aspfu-q4wk31, aspfu-q4wk44, aspfu-q4wk90, aspfu-q4wm12, aspfu-q4wm84, aspfu-q4wm86, aspfu-q4wmr0, aspfu-q4wny7, aspfu-q4wp19, aspfu-q4wpb9, aspfu-q4wqj8, aspfu-q4wqv2, aspfu-q4wrr7, aspfu-q4wu51, aspfu-q4wub2, aspfu-q4wui7, aspfu-q4wuk8, aspfu-q4wum3, aspfu-q4wuw0, aspfu-q4wvy1, aspfu-q4ww22, aspfu-q4wx13, aspfu-q4wxd0, aspfu-q4wxe4, aspfu-q4wxr1, aspfu-q4wyq5, aspfu-q4wz16, aspfu-q4wzd5, aspfu-q4wzh6, aspfu-q4x0n6, aspfu-q4x1n0, aspfu-q4x1w9, aspfu-q4x078, neofi-a1cwa6, neofi-a1d4m8, neofi-a1d4p0, neofi-a1d5p2, neofi-a1d104, neofi-a1d380, neofi-a1d512, neofi-a1d654, neofi-a1da18, neofi-a1dal8, neofi-a1df46, neofi-a1dhj0, neofi-a1di44, neofi-a1dk35, neofi-a1dki7, neofi-a1dkt6, neofi-a1dn55, neofi-atg15, neofi-axe1, neofi-faeb1, neofi-faeb2, neofi-faec, aspcl-a1cd34, aspcl-a1cd88, neofi-a1dc66, aspcl-a1ceh5, neofi-a1dfr9, aspfm-a0a084bf80, aspcl-a1cqb5, aspcl-a1cs44, neofi-a1d517, neofi-a1dbz0, neofi-a1cuz0, aspcl-a1c5e8, neofi-a1d0b8, aspcl-a1cdf0, aspcl-a1ccd3, neofi-a1da82, neofi-a1d5e6, aspcl-kex1, aspcl-cbpya Abstract We present the genome sequences of a new clinical isolate of the important human pathogen, Aspergillus fumigatus, A1163, and two closely related but rarely pathogenic species, Neosartorya fischeri NRRL181 and Aspergillus clavatus NRRL1. Comparative genomic analysis of A1163 with the recently sequenced A. fumigatus isolate Af293 has identified core, variable and up to 2% unique genes in each genome. While the core genes are 99.8% identical at the nucleotide level, identity for variable genes can be as low 40%. The most divergent loci appear to contain heterokaryon incompatibility (het) genes associated with fungal programmed cell death such as developmental regulator rosA. Cross-species comparison has revealed that 8.5%, 13.5% and 12.6%, respectively, of A. fumigatus, N. fischeri and A. clavatus genes are species-specific. These genes are significantly smaller in size than core genes, contain fewer exons and exhibit a subtelomeric bias. Most of them cluster together in 13 chromosomal islands, which are enriched for pseudogenes, transposons and other repetitive elements. At least 20% of A. fumigatus-specific genes appear to be functional and involved in carbohydrate and chitin catabolism, transport, detoxification, secondary metabolism and other functions that may facilitate the adaptation to heterogeneous environments such as soil or a mammalian host. Contrary to what was suggested previously, their origin cannot be attributed to horizontal gene transfer (HGT), but instead is likely to involve duplication, diversification and differential gene loss (DDL). The role of duplication in the origin of lineage-specific genes is further underlined by the discovery of genomic islands that seem to function as designated "gene dumps" and, perhaps, simultaneously, as "gene factories". Title: Draft genome sequence of the sexually transmitted pathogen Trichomonas vaginalis Carlton JM, Hirt RP, Silva JC, Delcher AL, Schatz M, Zhao Q, Wortman JR, Bidwell SL, Alsmark UC and Johnson PJ <55 more author(s)> Carlton JM, Hirt RP, Silva JC, Delcher AL, Schatz M, Zhao Q, Wortman JR, Bidwell SL, Alsmark UC, Besteiro S, Sicheritz-Ponten T, Noel CJ, Dacks JB, Foster PG, Simillion C, Van de Peer Y, Miranda-Saavedra D, Barton GJ, Westrop GD, Muller S, Dessi D, Fiori PL, Ren Q, Paulsen I, Zhang H, Bastida-Corcuera FD, Simoes-Barbosa A, Brown MT, Hayes RD, Mukherjee M, Okumura CY, Schneider R, Smith AJ, Vanacova S, Villalvazo M, Haas BJ, Pertea M, Feldblyum TV, Utterback TR, Shu CL, Osoegawa K, de Jong PJ, Hrdy I, Horvathova L, Zubacova Z, Dolezal P, Malik SB, Logsdon JM, Jr., Henze K, Gupta A, Wang CC, Dunne RL, Upcroft JA, Upcroft P, White O, Salzberg SL, Tang P, Chiu CH, Lee YS, Embley TM, Coombs GH, Mottram JC, Tachezy J, Fraser-Liggett CM, Johnson PJ (- 55) Ref: Science, 315:207, 2007 : PubMed ESTHER: Carlton_2007_Science_315_207 PubMedSearch: Carlton 2007 Science 315 207 PubMedID: 17218520 Gene_locus related to this paper: triva-a2d7i4, triva-a2d9w5, triva-a2d766, triva-a2dah5, triva-a2dlx9, triva-a2dul1, triva-a2dy49, triva-a2e6h5, triva-a2e7p9, triva-a2e9l3, triva-a2e414, triva-a2e613, triva-a2e983, triva-a2eau8, triva-a2ekb9, triva-a2en58, triva-a2erp5, triva-a2et59, triva-a2f7u4, triva-a2f801, triva-a2fa76, triva-a2fbq3, triva-a2fe47, triva-a2fgl0, triva-a2fhp7, triva-a2fie6, triva-a2fk22, triva-a2fla2, triva-a2fqm0, triva-a2fqq2, triva-a2frq0, triva-a2frr3, triva-a2fsq9, triva-a2fsz5, triva-a2fux4, triva-a2fz57, triva-a2g2h0, triva-a2g9x0, triva-a2fqi4 Abstract We describe the genome sequence of the protist Trichomonas vaginalis, a sexually transmitted human pathogen. Repeats and transposable elements comprise about two-thirds of the approximately 160-megabase genome, reflecting a recent massive expansion of genetic material. This expansion, in conjunction with the shaping of metabolic pathways that likely transpired through lateral gene transfer from bacteria, and amplification of specific gene families implicated in pathogenesis and phagocytosis of host proteins may exemplify adaptations of the parasite during its transition to a urogenital environment. The genome sequence predicts previously unknown functions for the hydrogenosome, which support a common evolutionary origin of this unusual organelle with mitochondria. Title: Macronuclear genome sequence of the ciliate Tetrahymena thermophila, a model eukaryote Eisen JA, Coyne RS, Wu M, Wu D, Thiagarajan M, Wortman JR, Badger JH, Ren Q, Amedeo P and Orias E <43 more author(s)> Eisen JA, Coyne RS, Wu M, Wu D, Thiagarajan M, Wortman JR, Badger JH, Ren Q, Amedeo P, Jones KM, Tallon LJ, Delcher AL, Salzberg SL, Silva JC, Haas BJ, Majoros WH, Farzad M, Carlton JM, Smith RK, Jr., Garg J, Pearlman RE, Karrer KM, Sun L, Manning G, Elde NC, Turkewitz AP, Asai DJ, Wilkes DE, Wang Y, Cai H, Collins K, Stewart BA, Lee SR, Wilamowska K, Weinberg Z, Ruzzo WL, Wloga D, Gaertig J, Frankel J, Tsao CC, Gorovsky MA, Keeling PJ, Waller RF, Patron NJ, Cherry JM, Stover NA, Krieger CJ, del Toro C, Ryder HF, Williamson SC, Barbeau RA, Hamilton EP, Orias E (- 43) Ref: PLoS Biol, 4:e286, 2006 : PubMed ESTHER: Eisen_2006_PLoS.Biol_4_e286 PubMedSearch: Eisen 2006 PLoS.Biol 4 e286 PubMedID: 16933976 Gene_locus related to this paper: tetts-i7mam3, tetts-i7ml33 Abstract The ciliate Tetrahymena thermophila is a model organism for molecular and cellular biology. Like other ciliates, this species has separate germline and soma functions that are embodied by distinct nuclei within a single cell. The germline-like micronucleus (MIC) has its genome held in reserve for sexual reproduction. The soma-like macronucleus (MAC), which possesses a genome processed from that of the MIC, is the center of gene expression and does not directly contribute DNA to sexual progeny. We report here the shotgun sequencing, assembly, and analysis of the MAC genome of T. thermophila, which is approximately 104 Mb in length and composed of approximately 225 chromosomes. Overall, the gene set is robust, with more than 27,000 predicted protein-coding genes, 15,000 of which have strong matches to genes in other organisms. The functional diversity encoded by these genes is substantial and reflects the complexity of processes required for a free-living, predatory, single-celled organism. This is highlighted by the abundance of lineage-specific duplications of genes with predicted roles in sensing and responding to environmental conditions (e.g., kinases), using diverse resources (e.g., proteases and transporters), and generating structural complexity (e.g., kinesins and dyneins). In contrast to the other lineages of alveolates (apicomplexans and dinoflagellates), no compelling evidence could be found for plastid-derived genes in the genome. UGA, the only T. thermophila stop codon, is used in some genes to encode selenocysteine, thus making this organism the first known with the potential to translate all 64 codons in nuclear genes into amino acids. We present genomic evidence supporting the hypothesis that the excision of DNA from the MIC to generate the MAC specifically targets foreign DNA as a form of genome self-defense. The combination of the genome sequence, the functional diversity encoded therein, and the presence of some pathways missing from other model organisms makes T. thermophila an ideal model for functional genomic studies to address biological, biomedical, and biotechnological questions of fundamental importance. Title: Comparative genomics of trypanosomatid parasitic protozoa El-Sayed NM, Myler PJ, Blandin G, Berriman M, Crabtree J, Aggarwal G, Caler E, Renauld H, Worthey EA and Hall N <35 more author(s)> El-Sayed NM, Myler PJ, Blandin G, Berriman M, Crabtree J, Aggarwal G, Caler E, Renauld H, Worthey EA, Hertz-Fowler C, Ghedin E, Peacock C, Bartholomeu DC, Haas BJ, Tran AN, Wortman JR, Alsmark UC, Angiuoli S, Anupama A, Badger J, Bringaud F, Cadag E, Carlton JM, Cerqueira GC, Creasy T, Delcher AL, Djikeng A, Embley TM, Hauser C, Ivens AC, Kummerfeld SK, Pereira-Leal JB, Nilsson D, Peterson J, Salzberg SL, Shallom J, Silva JC, Sundaram J, Westenberger S, White O, Melville SE, Donelson JE, Andersson B, Stuart KD, Hall N (- 35) Ref: Science, 309:404, 2005 : PubMed ESTHER: El-Sayed_2005_Science_309_404 PubMedSearch: El-Sayed 2005 Science 309 404 PubMedID: 16020724 Gene_locus related to this paper: tryb2-q382c1, trycr-q4dhv2, trycr-q4dpt2, trycr-q4dpy4 Abstract A comparison of gene content and genome architecture of Trypanosoma brucei, Trypanosoma cruzi, and Leishmania major, three related pathogens with different life cycles and disease pathology, revealed a conserved core proteome of about 6200 genes in large syntenic polycistronic gene clusters. Many species-specific genes, especially large surface antigen families, occur at nonsyntenic chromosome-internal and subtelomeric regions. Retroelements, structural RNAs, and gene family expansion are often associated with syntenic discontinuities that-along with gene divergence, acquisition and loss, and rearrangement within the syntenic regions-have shaped the genomes of each parasite. Contrary to recent reports, our analyses reveal no evidence that these species are descended from an ancestor that contained a photosynthetic endosymbiont. Title: Genome sequence of Theileria parva, a bovine pathogen that transforms lymphocytes Gardner MJ, Bishop R, Shah T, de Villiers EP, Carlton JM, Hall N, Ren Q, Paulsen IT, Pain A and Nene V <34 more author(s)> Gardner MJ, Bishop R, Shah T, de Villiers EP, Carlton JM, Hall N, Ren Q, Paulsen IT, Pain A, Berriman M, Wilson RJ, Sato S, Ralph SA, Mann DJ, Xiong Z, Shallom SJ, Weidman J, Jiang L, Lynn J, Weaver B, Shoaibi A, Domingo AR, Wasawo D, Crabtree J, Wortman JR, Haas B, Angiuoli SV, Creasy TH, Lu C, Suh B, Silva JC, Utterback TR, Feldblyum TV, Pertea M, Allen J, Nierman WC, Taracha EL, Salzberg SL, White OR, Fitzhugh HA, Morzaria S, Venter JC, Fraser CM, Nene V (- 34) Ref: Science, 309:134, 2005 : PubMed ESTHER: Gardner_2005_Science_309_134 PubMedSearch: Gardner 2005 Science 309 134 PubMedID: 15994558 Gene_locus related to this paper: thepa-q4mzr2, thepa-q4n0b4, thepa-q4n2i4, thepa-q4n4i8, thepa-q4n5d6, thepa-q4n5m4, thepa-q4n006, thepa-q4n9g7, thepa-q4n315, thepa-q4n349, thepa-q4n803 Abstract We report the genome sequence of Theileria parva, an apicomplexan pathogen causing economic losses to smallholder farmers in Africa. The parasite chromosomes exhibit limited conservation of gene synteny with Plasmodium falciparum, and its plastid-like genome represents the first example where all apicoplast genes are encoded on one DNA strand. We tentatively identify proteins that facilitate parasite segregation during host cell cytokinesis and contribute to persistent infection of transformed host cells. Several biosynthetic pathways are incomplete or absent, suggesting substantial metabolic dependence on the host cell. One protein family that may generate parasite antigenic diversity is not telomere-associated. Title: Genome sequence and comparative analysis of the model rodent malaria parasite Plasmodium yoelii yoelii Carlton JM, Angiuoli SV, Suh BB, Kooij TW, Pertea M, Silva JC, Ermolaeva MD, Allen JE, Selengut JD and Carucci DJ <34 more author(s)> Carlton JM, Angiuoli SV, Suh BB, Kooij TW, Pertea M, Silva JC, Ermolaeva MD, Allen JE, Selengut JD, Koo HL, Peterson JD, Pop M, Kosack DS, Shumway MF, Bidwell SL, Shallom SJ, Van Aken SE, Riedmuller SB, Feldblyum TV, Cho JK, Quackenbush J, Sedegah M, Shoaibi A, Cummings LM, Florens L, Yates JR, Raine JD, Sinden RE, Harris MA, Cunningham DA, Preiser PR, Bergman LW, Vaidya AB, van Lin LH, Janse CJ, Waters AP, Smith HO, White OR, Salzberg SL, Venter JC, Fraser CM, Hoffman SL, Gardner MJ, Carucci DJ (- 34) Ref: Nature, 419:512, 2002 : PubMed ESTHER: Carlton_2002_Nature_419_512 PubMedSearch: Carlton 2002 Nature 419 512 PubMedID: 12368865 Gene_locus related to this paper: playo-PY04076, playo-PY04938, playo-PY05572, playo-q7pdu6, playo-q7r7y2, playo-q7rbj8, playo-q7rdk4, playo-q7rgi9, playo-q7rh25, playo-q7rki0, playo-q7rl68, playo-q7rl69, playo-q7rmm1, playo-q7rn16, playo-q7rpk0, playo-q7rq09, playo-q7rq49, playo-q7rq68 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. Title: Heterologous expression, isolation, and characterization of versicolorin B synthase from Aspergillus parasiticus. A key enzyme in the aflatoxin B1 biosynthetic pathway Silva JC, Townsend CA Ref: Journal of Biological Chemistry, 272:804, 1997 : PubMed ESTHER: Silva_1997_J.Biol.Chem_272_804 PubMedSearch: Silva 1997 J.Biol.Chem 272 804 PubMedID: 8995367 Abstract Aflatoxin B1 is a potent environmental carcinogen produced by certain strains of Aspergillus. Central to the biosynthesis of this mycotoxin is the reaction catalyzed by versicolorin B synthase (VBS) in which a racemic substrate, versiconal hemiacetal, is cyclized to an optically active product whose absolute configuration is crucial to the interaction of aflatoxin B1 with DNA. Attempted over-production of VBS in Escherichia coli led principally to protein aggregated into inclusion bodies but also small amounts of soluble but catalytically inactive enzyme. Comparisons to wild-type VBS by SDS-polyacrylamide gel electrophoresis and after N-glycosidase F treatment revealed that extensive glycosylation accounted for the mass discrepancy (7,000+/-1,500 Da) between the native and bacterially expressed proteins. Several over-expression systems in Saccharomyces cerevisiae were surveyed in which one that incorporated a secretion signal was found most successful. VBS of indistinguishable mass on SDS-polyacrylamide gel electrophoresis and kinetic properties from the wild-type enzyme could be obtained in 50-100-fold greater amounts and whose catalytic behavior has been examined. The translated protein sequence of VBS showed three potential N-glycosylation sites (Asn-Xaa-Ser/Thr) consistent with the modifications observed above and unexpectedly revealed extensive homology to the ADP-binding region prominently conserved in the glucose-methanol-choline (GMC) family of flavoenzymes. Over-production of VBS in yeast marks the first aflatoxin biosynthetic enzyme to be so obtained and opens the way to direct study of the enzymology of this complex biosynthetic pathway. | |||||||
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