Author Report for: Moule SNo contact information in database for Moule S
Pain A, Bohme U, Berry AE, Mungall K, Finn RD, Jackson AP, Mourier T, Mistry J, Pasini EM and Berriman M <44 more author(s)> Pain A, Bohme U, Berry AE, Mungall K, Finn RD, Jackson AP, Mourier T, Mistry J, Pasini EM, Aslett MA, Balasubrammaniam S, Borgwardt K, Brooks K, Carret C, Carver TJ, Cherevach I, Chillingworth T, Clark TG, Galinski MR, Hall N, Harper D, Harris D, Hauser H, Ivens A, Janssen CS, Keane T, Larke N, Lapp S, Marti M, Moule S, Meyer IM, Ormond D, Peters N, Sanders M, Sanders S, Sargeant TJ, Simmonds M, Smith F, Squares R, Thurston S, Tivey AR, Walker D, White B, Zuiderwijk E, Churcher C, Quail MA, Cowman AF, Turner CM, Rajandream MA, Kocken CH, Thomas AW, Newbold CI, Barrell BG, Berriman M (- 44) Ref: Nature, 455:799, 2008 : PubMed ESTHER: Pain_2008_Nature_455_799 PubMedSearch: Pain 2008 Nature 455 799 PubMedID: 18843368 Gene_locus related to this paper: plakh-b3kz42, plakh-b3kz45, plakh-b3l0y4, plakh-b3l1r3, plakh-b3l8u5, plakh-b3l336, plakh-b3l571, plakh-b3la01, plakh-b3lb44 Abstract Plasmodium knowlesi is an intracellular malaria parasite whose natural vertebrate host is Macaca fascicularis (the 'kra' monkey); however, it is now increasingly recognized as a significant cause of human malaria, particularly in southeast Asia. Plasmodium knowlesi was the first malaria parasite species in which antigenic variation was demonstrated, and it has a close phylogenetic relationship to Plasmodium vivax, the second most important species of human malaria parasite (reviewed in ref. 4). Despite their relatedness, there are important phenotypic differences between them, such as host blood cell preference, absence of a dormant liver stage or 'hypnozoite' in P. knowlesi, and length of the asexual cycle (reviewed in ref. 4). Here we present an analysis of the P. knowlesi (H strain, Pk1(A+) clone) nuclear genome sequence. This is the first monkey malaria parasite genome to be described, and it provides an opportunity for comparison with the recently completed P. vivax genome and other sequenced Plasmodium genomes. In contrast to other Plasmodium genomes, putative variant antigen families are dispersed throughout the genome and are associated with intrachromosomal telomere repeats. One of these families, the KIRs, contains sequences that collectively match over one-half of the host CD99 extracellular domain, which may represent an unusual form of molecular mimicry. Title: Complete genome sequence of uropathogenic Proteus mirabilis, a master of both adherence and motility Pearson MM, Sebaihia M, Churcher C, Quail MA, Seshasayee AS, Luscombe NM, Abdellah Z, Arrosmith C, Atkin B and Mobley HL <12 more author(s)> Pearson MM, Sebaihia M, Churcher C, Quail MA, Seshasayee AS, Luscombe NM, Abdellah Z, Arrosmith C, Atkin B, Chillingworth T, Hauser H, Jagels K, Moule S, Mungall K, Norbertczak H, Rabbinowitsch E, Walker D, Whithead S, Thomson NR, Rather PN, Parkhill J, Mobley HL (- 12) Ref: Journal of Bacteriology, 190:4027, 2008 : PubMed ESTHER: Pearson_2008_J.Bacteriol_190_4027 PubMedSearch: Pearson 2008 J.Bacteriol 190 4027 PubMedID: 18375554 Gene_locus related to this paper: promh-b4euu8, promh-b4ev30, promh-b4evj5, promh-b4f0a1, promh-bioh, promi-c2lhp6, promi-c2lla8, promi-NRPS, promi-NRPT, promi-k1gzm2, promh-b4eve8 Abstract The gram-negative enteric bacterium Proteus mirabilis is a frequent cause of urinary tract infections in individuals with long-term indwelling catheters or with complicated urinary tracts (e.g., due to spinal cord injury or anatomic abnormality). P. mirabilis bacteriuria may lead to acute pyelonephritis, fever, and bacteremia. Most notoriously, this pathogen uses urease to catalyze the formation of kidney and bladder stones or to encrust or obstruct indwelling urinary catheters. Here we report the complete genome sequence of P. mirabilis HI4320, a representative strain cultured in our laboratory from the urine of a nursing home patient with a long-term (> or =30 days) indwelling urinary catheter. The genome is 4.063 Mb long and has a G+C content of 38.88%. There is a single plasmid consisting of 36,289 nucleotides. Annotation of the genome identified 3,685 coding sequences and seven rRNA loci. Analysis of the sequence confirmed the presence of previously identified virulence determinants, as well as a contiguous 54-kb flagellar regulon and 17 types of fimbriae. Genes encoding a potential type III secretion system were identified on a low-G+C-content genomic island containing 24 intact genes that appear to encode all components necessary to assemble a type III secretion system needle complex. In addition, the P. mirabilis HI4320 genome possesses four tandem copies of the zapE metalloprotease gene, genes encoding six putative autotransporters, an extension of the atf fimbrial operon to six genes, including an mrpJ homolog, and genes encoding at least five iron uptake mechanisms, two potential type IV secretion systems, and 16 two-component regulators. Title: Insights from the complete genome sequence of Mycobacterium marinum on the evolution of Mycobacterium tuberculosis Stinear TP, Seemann T, Harrison PF, Jenkin GA, Davies JK, Johnson PD, Abdellah Z, Arrowsmith C, Chillingworth T and Cole ST <21 more author(s)> Stinear TP, Seemann T, Harrison PF, Jenkin GA, Davies JK, Johnson PD, Abdellah Z, Arrowsmith C, Chillingworth T, Churcher C, Clarke K, Cronin A, Davis P, Goodhead I, Holroyd N, Jagels K, Lord A, Moule S, Mungall K, Norbertczak H, Quail MA, Rabbinowitsch E, Walker D, White B, Whitehead S, Small PL, Brosch R, Ramakrishnan L, Fischbach MA, Parkhill J, Cole ST (- 21) Ref: Genome Res, 18:729, 2008 : PubMed ESTHER: Stinear_2008_Genome.Res_18_729 PubMedSearch: Stinear 2008 Genome.Res 18 729 PubMedID: 18403782 Gene_locus related to this paper: mycmm-b2hds9, mycmm-b2hed7, mycmm-b2hg81, mycmm-b2hgg2, mycmm-b2hgg7, mycmm-b2hhi7, mycmm-b2hhu3, mycmm-b2hiu3, mycmm-b2hiu5, mycmm-b2hiw7, mycmm-b2hiy0, mycmm-b2hj55, mycmm-b2hjb4, mycmm-b2hju3, mycmm-b2hku1, mycmm-b2hkw0, mycmm-b2hlr0, mycmm-b2hlt7, mycmm-b2hlt8, mycmm-b2hlt9, mycmm-b2hlu0, mycmm-b2hlv0, mycmm-b2hlv1, mycmm-b2hlv2, mycmm-b2hlx2, mycmm-b2hm55, mycmm-b2hnr9, mycmm-b2hnz5, mycmm-b2hp80, mycmm-b2hpp0, mycmm-b2hq96, mycmm-b2hr10, mycmm-b2hsm6, mycmm-b2hsm8, mycmm-b2hsy0, mycmm-b2ht06, mycmm-b2ht20, mycmm-b2ht49, mycmm-dhma, mycmm-metx, mycmr-q5sdq4, myctu-RV1683, mycmm-b2h1k1, mycua-a0pku2, mycua-a0pl47, mycua-a0plr3, mycua-a0pm12, mycua-a0pm14, mycua-a0pmv0, mycua-a0pmx9, mycua-a0pn71, mycua-a0ppm6, mycua-a0pqm2, mycua-a0pqs2, mycua-a0prq2, mycua-a0psb1, mycua-a0psb4, mycua-a0psi2, mycua-a0pth6, mycua-a0ptq0, mycua-a0pu55, mycua-a0pum4, mycua-a0pv11, mycua-a0pva4, mycua-a0pwi8, mycua-a0pwr6, mycua-a0pwz5, mycul-a85a, mycmm-b2hcy1, mycua-a0pvg7, mycmm-b2hnj4, mycmm-b2he93, mycua-a0pwz4, mycmm-b2hqy3, mycua-a0pmc3, mycmm-b2hnn7, mycmm-b2he68, mycmm-b2hqm3, mycmm-tesa Abstract Mycobacterium marinum, a ubiquitous pathogen of fish and amphibia, is a near relative of Mycobacterium tuberculosis, the etiologic agent of tuberculosis in humans. The genome of the M strain of M. marinum comprises a 6,636,827-bp circular chromosome with 5424 CDS, 10 prophages, and a 23-kb mercury-resistance plasmid. Prominent features are the very large number of genes (57) encoding polyketide synthases (PKSs) and nonribosomal peptide synthases (NRPSs) and the most extensive repertoire yet reported of the mycobacteria-restricted PE and PPE proteins, and related-ESX secretion systems. Some of the NRPS genes comprise a novel family and seem to have been acquired horizontally. M. marinum is used widely as a model organism to study M. tuberculosis pathogenesis, and genome comparisons confirmed the close genetic relationship between these two species, as they share 3000 orthologs with an average amino acid identity of 85%. Comparisons with the more distantly related Mycobacterium avium subspecies paratuberculosis and Mycobacterium smegmatis reveal how an ancestral generalist mycobacterium evolved into M. tuberculosis and M. marinum. M. tuberculosis has undergone genome downsizing and extensive lateral gene transfer to become a specialized pathogen of humans and other primates without retaining an environmental niche. M. marinum has maintained a large genome so as to retain the capacity for environmental survival while becoming a broad host range pathogen that produces disease strikingly similar to M. tuberculosis. The work described herein provides a foundation for using M. marinum to better understand the determinants of pathogenesis of tuberculosis. Title: Comparative genome analysis of Salmonella Enteritidis PT4 and Salmonella Gallinarum 287/91 provides insights into evolutionary and host adaptation pathways Thomson NR, Clayton DJ, Windhorst D, Vernikos G, Davidson S, Churcher C, Quail MA, Stevens M, Jones MA and Parkhill J <28 more author(s)> Thomson NR, Clayton DJ, Windhorst D, Vernikos G, Davidson S, Churcher C, Quail MA, Stevens M, Jones MA, Watson M, Barron A, Layton A, Pickard D, Kingsley RA, Bignell A, Clark L, Harris B, Ormond D, Abdellah Z, Brooks K, Cherevach I, Chillingworth T, Woodward J, Norberczak H, Lord A, Arrowsmith C, Jagels K, Moule S, Mungall K, Sanders M, Whitehead S, Chabalgoity JA, Maskell D, Humphrey T, Roberts M, Barrow PA, Dougan G, Parkhill J (- 28) Ref: Genome Res, 18:1624, 2008 : PubMed ESTHER: Thomson_2008_Genome.Res_18_1624 PubMedSearch: Thomson 2008 Genome.Res 18 1624 PubMedID: 18583645 Gene_locus related to this paper: salen-OPDB, salti-q8z717, salty-AES, salty-BIOH, salty-DLHH, salty-ENTF, salty-FES, salty-IROD, salty-IROE, salty-P74847, salty-PLDB, salty-STM0332, salty-STM4506, salty-STY1441, salty-STY2428, salty-STY3846, salty-yafa, salty-YBFF, salty-ycfp, salty-YFBB, salty-YHET, salty-YQIA Abstract We have determined the complete genome sequences of a host-promiscuous Salmonella enterica serovar Enteritidis PT4 isolate P125109 and a chicken-restricted Salmonella enterica serovar Gallinarum isolate 287/91. Genome comparisons between these and other Salmonella isolates indicate that S. Gallinarum 287/91 is a recently evolved descendent of S. Enteritidis. Significantly, the genome of S. Gallinarum has undergone extensive degradation through deletion and pseudogene formation. Comparison of the pseudogenes in S. Gallinarum with those identified previously in other host-adapted bacteria reveals the loss of many common functional traits and provides insights into possible mechanisms of host and tissue adaptation. We propose that experimental analysis in chickens and mice of S. Enteritidis-harboring mutations in functional homologs of the pseudogenes present in S. Gallinarum could provide an experimentally tractable route toward unraveling the genetic basis of host adaptation in S. enterica. Title: Meningococcal genetic variation mechanisms viewed through comparative analysis of serogroup C strain FAM18 Bentley SD, Vernikos GS, Snyder LA, Churcher C, Arrowsmith C, Chillingworth T, Cronin A, Davis PH, Holroyd NE and Parkhill J <11 more author(s)> Bentley SD, Vernikos GS, Snyder LA, Churcher C, Arrowsmith C, Chillingworth T, Cronin A, Davis PH, Holroyd NE, Jagels K, Maddison M, Moule S, Rabbinowitsch E, Sharp S, Unwin L, Whitehead S, Quail MA, Achtman M, Barrell B, Saunders NJ, Parkhill J (- 11) Ref: PLoS Genet, 3:e23, 2007 : PubMed ESTHER: Bentley_2007_PLoS.Genet_3_e23 PubMedSearch: Bentley 2007 PLoS.Genet 3 e23 PubMedID: 17305430 Gene_locus related to this paper: neigo-pip, neima-metx, neimb-q9k0t9, neime-ESD, neime-NMA2216, neime-NMB0276, neime-NMB1828, neime-NMB1877, neimf-a1kta9 Abstract The bacterium Neisseria meningitidis is commonly found harmlessly colonising the mucosal surfaces of the human nasopharynx. Occasionally strains can invade host tissues causing septicaemia and meningitis, making the bacterium a major cause of morbidity and mortality in both the developed and developing world. The species is known to be diverse in many ways, as a product of its natural transformability and of a range of recombination and mutation-based systems. Previous work on pathogenic Neisseria has identified several mechanisms for the generation of diversity of surface structures, including phase variation based on slippage-like mechanisms and sequence conversion of expressed genes using information from silent loci. Comparison of the genome sequences of two N. meningitidis strains, serogroup B MC58 and serogroup A Z2491, suggested further mechanisms of variation, including C-terminal exchange in specific genes and enhanced localised recombination and variation related to repeat arrays. We have sequenced the genome of N. meningitidis strain FAM18, a representative of the ST-11/ET-37 complex, providing the first genome sequence for the disease-causing serogroup C meningococci; it has 1,976 predicted genes, of which 60 do not have orthologues in the previously sequenced serogroup A or B strains. Through genome comparison with Z2491 and MC58 we have further characterised specific mechanisms of genetic variation in N. meningitidis, describing specialised loci for generation of cell surface protein variants and measuring the association between noncoding repeat arrays and sequence variation in flanking genes. Here we provide a detailed view of novel genetic diversification mechanisms in N. meningitidis. Our analysis provides evidence for the hypothesis that the noncoding repeat arrays in neisserial genomes (neisserial intergenic mosaic elements) provide a crucial mechanism for the generation of surface antigen variants. Such variation will have an impact on the interaction with the host tissues, and understanding these mechanisms is important to aid our understanding of the intimate and complex relationship between the human nasopharynx and the meningococcus. Title: Complete genome of acute rheumatic fever-associated serotype M5 Streptococcus pyogenes strain manfredo Holden MT, Scott A, Cherevach I, Chillingworth T, Churcher C, Cronin A, Dowd L, Feltwell T, Hamlin N and Parkhill J <12 more author(s)> Holden MT, Scott A, Cherevach I, Chillingworth T, Churcher C, Cronin A, Dowd L, Feltwell T, Hamlin N, Holroyd S, Jagels K, Moule S, Mungall K, Quail MA, Price C, Rabbinowitsch E, Sharp S, Skelton J, Whitehead S, Barrell BG, Kehoe M, Parkhill J (- 12) Ref: Journal of Bacteriology, 189:1473, 2007 : PubMed ESTHER: Holden_2007_J.Bacteriol_189_1473 PubMedSearch: Holden 2007 J.Bacteriol 189 1473 PubMedID: 17012393 Gene_locus related to this paper: strpy-ESTA, strpy-PEPXP, strpy-SPY1308, strpy-SPYM18.1727 Abstract Comparisons of the 1.84-Mb genome of serotype M5 Streptococcus pyogenes strain Manfredo with previously sequenced genomes emphasized the role of prophages in diversification of S. pyogenes and the close relationship between strain Manfredo and MGAS8232, another acute rheumatic fever-associated strain. Title: Comparative genomic analysis of three Leishmania species that cause diverse human disease Peacock CS, Seeger K, Harris D, Murphy L, Ruiz JC, Quail MA, Peters N, Adlem E, Tivey A and Berriman M <32 more author(s)> Peacock CS, Seeger K, Harris D, Murphy L, Ruiz JC, Quail MA, Peters N, Adlem E, Tivey A, Aslett M, Kerhornou A, Ivens A, Fraser A, Rajandream MA, Carver T, Norbertczak H, Chillingworth T, Hance Z, Jagels K, Moule S, Ormond D, Rutter S, Squares R, Whitehead S, Rabbinowitsch E, Arrowsmith C, White B, Thurston S, Bringaud F, Baldauf SL, Faulconbridge A, Jeffares D, Depledge DP, Oyola SO, Hilley JD, Brito LO, Tosi LR, Barrell B, Cruz AK, Mottram JC, Smith DF, Berriman M (- 32) Ref: Nat Genet, 39:839, 2007 : PubMed ESTHER: Peacock_2007_Nat.Genet_39_839 PubMedSearch: Peacock 2007 Nat.Genet 39 839 PubMedID: 17572675 Gene_locus related to this paper: leibr-a4h6l0, leibr-a4h6l1, leibr-a4h9b6, leibr-a4h908, leibr-a4h956, leibr-a4h959, leibr-a4h960, leibr-a4hen1, leibr-a4hf07, leibr-a4hgl0, leibr-a4hhu6, leibr-a4hj94, leibr-a4hk72, leibr-a4hpa8, leibr-a4hpz5, leiin-a4huz4, leiin-a4hxe0, leiin-a4hxh8, leiin-a4hxi1, leiin-a4hxn7, leiin-a4hyv9, leiin-a4i1v9, leiin-a4i4z6, leiin-a4i6n9, leiin-a4i7q7, leiin-a4idl6, leima-e9ady6, leima-OPB, leima-q4q0t5, leima-q4q8a8, leima-q4q398, leima-q4q942, leima-q4qe85, leima-q4qe86, leima-q4qj45 Abstract Leishmania parasites cause a broad spectrum of clinical disease. Here we report the sequencing of the genomes of two species of Leishmania: Leishmania infantum and Leishmania braziliensis. The comparison of these sequences with the published genome of Leishmania major reveals marked conservation of synteny and identifies only approximately 200 genes with a differential distribution between the three species. L. braziliensis, contrary to Leishmania species examined so far, possesses components of a putative RNA-mediated interference pathway, telomere-associated transposable elements and spliced leader-associated SLACS retrotransposons. We show that pseudogene formation and gene loss are the principal forces shaping the different genomes. Genes that are differentially distributed between the species encode proteins implicated in host-pathogen interactions and parasite survival in the macrophage. Title: Genome sequence of a proteolytic (Group I) Clostridium botulinum strain Hall A and comparative analysis of the clostridial genomes Sebaihia M, Peck MW, Minton NP, Thomson NR, Holden MT, Mitchell WJ, Carter AT, Bentley SD, Mason DR and Parkhill J <24 more author(s)> Sebaihia M, Peck MW, Minton NP, Thomson NR, Holden MT, Mitchell WJ, Carter AT, Bentley SD, Mason DR, Crossman L, Paul CJ, Ivens A, Wells-Bennik MH, Davis IJ, Cerdeno-Tarraga AM, Churcher C, Quail MA, Chillingworth T, Feltwell T, Fraser A, Goodhead I, Hance Z, Jagels K, Larke N, Maddison M, Moule S, Mungall K, Norbertczak H, Rabbinowitsch E, Sanders M, Simmonds M, White B, Whithead S, Parkhill J (- 24) Ref: Genome Res, 17:1082, 2007 : PubMed ESTHER: Sebaihia_2007_Genome.Res_17_1082 PubMedSearch: Sebaihia 2007 Genome.Res 17 1082 PubMedID: 17519437 Gene_locus related to this paper: clobh-A5I3I2, clobh-A51055, clob1-a7fqm2, clob1-a7fv94, clobl-a7gbn0, clobh-pip, clobh-a5i3m0 Abstract Clostridium botulinum is a heterogeneous Gram-positive species that comprises four genetically and physiologically distinct groups of bacteria that share the ability to produce botulinum neurotoxin, the most poisonous toxin known to man, and the causative agent of botulism, a severe disease of humans and animals. We report here the complete genome sequence of a representative of Group I (proteolytic) C. botulinum (strain Hall A, ATCC 3502). The genome consists of a chromosome (3,886,916 bp) and a plasmid (16,344 bp), which carry 3650 and 19 predicted genes, respectively. Consistent with the proteolytic phenotype of this strain, the genome harbors a large number of genes encoding secreted proteases and enzymes involved in uptake and metabolism of amino acids. The genome also reveals a hitherto unknown ability of C. botulinum to degrade chitin. There is a significant lack of recently acquired DNA, indicating a stable genomic content, in strong contrast to the fluid genome of Clostridium difficile, which can form longer-term relationships with its host. Overall, the genome indicates that C. botulinum is adapted to a saprophytic lifestyle both in soil and aquatic environments. This pathogen relies on its toxin to rapidly kill a wide range of prey species, and to gain access to nutrient sources, it releases a large number of extracellular enzymes to soften and destroy rotting or decayed tissues. Title: Common inheritance of chromosome Ia associated with clonal expansion of Toxoplasma gondii Khan A, Bohme U, Kelly KA, Adlem E, Brooks K, Simmonds M, Mungall K, Quail MA, Arrowsmith C and Ajioka JW <29 more author(s)> Khan A, Bohme U, Kelly KA, Adlem E, Brooks K, Simmonds M, Mungall K, Quail MA, Arrowsmith C, Chillingworth T, Churcher C, Harris D, Collins M, Fosker N, Fraser A, Hance Z, Jagels K, Moule S, Murphy L, O'Neil S, Rajandream MA, Saunders D, Seeger K, Whitehead S, Mayr T, Xuan X, Watanabe J, Suzuki Y, Wakaguri H, Sugano S, Sugimoto C, Paulsen I, Mackey AJ, Roos DS, Hall N, Berriman M, Barrell B, Sibley LD, Ajioka JW (- 29) Ref: Genome Res, 16:1119, 2006 : PubMed ESTHER: Khan_2006_Genome.Res_16_1119 PubMedSearch: Khan 2006 Genome.Res 16 1119 PubMedID: 16902086 Gene_locus related to this paper: toxgo-q1jt22 Abstract Toxoplasma gondii is a globally distributed protozoan parasite that can infect virtually all warm-blooded animals and humans. Despite the existence of a sexual phase in the life cycle, T. gondii has an unusual population structure dominated by three clonal lineages that predominate in North America and Europe, (Types I, II, and III). These lineages were founded by common ancestors approximately10,000 yr ago. The recent origin and widespread distribution of the clonal lineages is attributed to the circumvention of the sexual cycle by a new mode of transmission-asexual transmission between intermediate hosts. Asexual transmission appears to be multigenic and although the specific genes mediating this trait are unknown, it is predicted that all members of the clonal lineages should share the same alleles. Genetic mapping studies suggested that chromosome Ia was unusually monomorphic compared with the rest of the genome. To investigate this further, we sequenced chromosome Ia and chromosome Ib in the Type I strain, RH, and the Type II strain, ME49. Comparative genome analyses of the two chromosomal sequences revealed that the same copy of chromosome Ia was inherited in each lineage, whereas chromosome Ib maintained the same high frequency of between-strain polymorphism as the rest of the genome. Sampling of chromosome Ia sequence in seven additional representative strains from the three clonal lineages supports a monomorphic inheritance, which is unique within the genome. Taken together, our observations implicate a specific combination of alleles on chromosome Ia in the recent origin and widespread success of the clonal lineages of T. gondii. Title: The multidrug-resistant human pathogen Clostridium difficile has a highly mobile, mosaic genome Sebaihia M, Wren BW, Mullany P, Fairweather NF, Minton N, Stabler R, Thomson NR, Roberts AP, Cerdeno-Tarraga AM and Parkhill J <29 more author(s)> Sebaihia M, Wren BW, Mullany P, Fairweather NF, Minton N, Stabler R, Thomson NR, Roberts AP, Cerdeno-Tarraga AM, Wang H, Holden MT, Wright A, Churcher C, Quail MA, Baker S, Bason N, Brooks K, Chillingworth T, Cronin A, Davis P, Dowd L, Fraser A, Feltwell T, Hance Z, Holroyd S, Jagels K, Moule S, Mungall K, Price C, Rabbinowitsch E, Sharp S, Simmonds M, Stevens K, Unwin L, Whithead S, Dupuy B, Dougan G, Barrell B, Parkhill J (- 29) Ref: Nat Genet, 38:779, 2006 : PubMed ESTHER: Sebaihia_2006_Nat.Genet_38_779 PubMedSearch: Sebaihia 2006 Nat.Genet 38 779 PubMedID: 16804543 Gene_locus related to this paper: pepdi-t4eki5, clod6-q18a60, clod6-q183v0, clodi-HYDD, clodr-c9ynf2, pepd6-pip, pepdi-g6brr4 Abstract We determined the complete genome sequence of Clostridium difficile strain 630, a virulent and multidrug-resistant strain. Our analysis indicates that a large proportion (11%) of the genome consists of mobile genetic elements, mainly in the form of conjugative transposons. These mobile elements are putatively responsible for the acquisition by C. difficile of an extensive array of genes involved in antimicrobial resistance, virulence, host interaction and the production of surface structures. The metabolic capabilities encoded in the genome show multiple adaptations for survival and growth within the gut environment. The extreme genome variability was confirmed by whole-genome microarray analysis; it may reflect the organism's niche in the gut and should provide information on the evolution of virulence in this organism. Title: The complete genome sequence and comparative genome analysis of the high pathogenicity Yersinia enterocolitica strain 8081 Thomson NR, Howard S, Wren BW, Holden MT, Crossman L, Challis GL, Churcher C, Mungall K, Brooks K and Prentice MB <12 more author(s)> Thomson NR, Howard S, Wren BW, Holden MT, Crossman L, Challis GL, Churcher C, Mungall K, Brooks K, Chillingworth T, Feltwell T, Abdellah Z, Hauser H, Jagels K, Maddison M, Moule S, Sanders M, Whitehead S, Quail MA, Dougan G, Parkhill J, Prentice MB (- 12) Ref: PLoS Genet, 2:e206, 2006 : PubMed ESTHER: Thomson_2006_PLoS.Genet_2_e206 PubMedSearch: Thomson 2006 PLoS.Genet 2 e206 PubMedID: 17173484 Gene_locus related to this paper: yere8-a1jik0, yere8-a1jmx1, yere8-a1jrp7, yere8-bioh, yere8-menh, yere8-y3204, yeren-fes, yeren-YPLA, yeren-YqiA, yermo-c4sfz7, yerpe-y1616, yerpe-YPO1501, yerbe-c4rym7 Abstract The human enteropathogen, Yersinia enterocolitica, is a significant link in the range of Yersinia pathologies extending from mild gastroenteritis to bubonic plague. Comparison at the genomic level is a key step in our understanding of the genetic basis for this pathogenicity spectrum. Here we report the genome of Y. enterocolitica strain 8081 (serotype 0:8; biotype 1B) and extensive microarray data relating to the genetic diversity of the Y. enterocolitica species. Our analysis reveals that the genome of Y. enterocolitica strain 8081 is a patchwork of horizontally acquired genetic loci, including a plasticity zone of 199 kb containing an extraordinarily high density of virulence genes. Microarray analysis has provided insights into species-specific Y. enterocolitica gene functions and the intraspecies differences between the high, low, and nonpathogenic Y. enterocolitica biotypes. Through comparative genome sequence analysis we provide new information on the evolution of the Yersinia. We identify numerous loci that represent ancestral clusters of genes potentially important in enteric survival and pathogenesis, which have been lost or are in the process of being lost, in the other sequenced Yersinia lineages. Our analysis also highlights large metabolic operons in Y. enterocolitica that are absent in the related enteropathogen, Yersinia pseudotuberculosis, indicating major differences in niche and nutrients used within the mammalian gut. These include clusters directing, the production of hydrogenases, tetrathionate respiration, cobalamin synthesis, and propanediol utilisation. Along with ancestral gene clusters, the genome of Y. enterocolitica has revealed species-specific and enteropathogen-specific loci. This has provided important insights into the pathology of this bacterium and, more broadly, into the evolution of the genus. Moreover, wider investigations looking at the patterns of gene loss and gain in the Yersinia have highlighted common themes in the genome evolution of other human enteropathogens. Title: The genome of Rhizobium leguminosarum has recognizable core and accessory components Young JP, Crossman LC, Johnston AW, Thomson NR, Ghazoui ZF, Hull KH, Wexler M, Curson AR, Todd JD and Parkhill J <22 more author(s)> Young JP, Crossman LC, Johnston AW, Thomson NR, Ghazoui ZF, Hull KH, Wexler M, Curson AR, Todd JD, Poole PS, Mauchline TH, East AK, Quail MA, Churcher C, Arrowsmith C, Cherevach I, Chillingworth T, Clarke K, Cronin A, Davis P, Fraser A, Hance Z, Hauser H, Jagels K, Moule S, Mungall K, Norbertczak H, Rabbinowitsch E, Sanders M, Simmonds M, Whitehead S, Parkhill J (- 22) Ref: Genome Biol, 7:R34, 2006 : PubMed ESTHER: Young_2006_Genome.Biol_7_R34 PubMedSearch: Young 2006 Genome.Biol 7 R34 PubMedID: 16640791 Gene_locus related to this paper: rhiec-q2k7y0, rhiec-q2k107, rhiec-q2kav5, rhiec-q2ke86, rhil3-q1m3b7, rhil3-q1m3u0, rhil3-q1m4b4, rhil3-q1m4e5, rhil3-q1m4g3, rhil3-q1m4h0, rhil3-q1m5k0, rhil3-q1m5s6, rhil3-q1m6q0, rhil3-q1m6u8, rhil3-q1m6w8, rhil3-q1m7c2, rhil3-q1m7c3, rhil3-q1m7i2, rhil3-q1m7n3, rhil3-q1m7q9, rhil3-q1m7r8, rhil3-q1m8d0, rhil3-q1m8u4, rhil3-q1m9d6, rhil3-q1m9i6, rhil3-q1m347, rhil3-q1m571, rhil3-q1m580, rhil3-q1m672, rhil3-q1m812, rhil3-q1m841, rhil3-q1m917, rhil3-q1m919, rhil3-q1mbv4, rhil3-q1mbz5, rhil3-q1mc48, rhil3-q1mcr4, rhil3-q1md19, rhil3-q1mdd8, rhil3-q1me05, rhil3-q1mee4, rhil3-q1mel6, rhil3-q1men7, rhil3-q1mf17, rhil3-q1mf73, rhil3-q1mf76, rhil3-q1mfb0, rhil3-q1mfp5, rhil3-q1mg17, rhil3-q1mg51, rhil3-q1mg97, rhil3-q1mgh3, rhil3-q1mgh5, rhil3-q1mgu7, rhil3-q1mgx5, rhil3-q1mh67, rhil3-q1mhh7, rhil3-q1mhz8, rhil3-q1mi67, rhil3-q1mi98, rhil3-q1mia3, rhil3-q1mig2, rhil3-q1miz0, rhil3-q1mj26, rhil3-q1mj65, rhil3-q1mjs2, rhil3-q1mjx4, rhil3-q1mk84, rhil3-q1mkk8, rhil3-q1mli7, rhil3-q1mlj7, rhil3-q1mm33, rhil3-q1mmf9, rhil3-q1mmp7, rhil3-q1mmx0, rhil3-q1mn42, rhile-Q93EA8, rhils-c6axl5, rhils-c6b1w7, rhilw-b5zrm4, rhilw-b5zs97, rhilv-j0vcs5 Abstract BACKGROUND: Rhizobium leguminosarum is an alpha-proteobacterial N2-fixing symbiont of legumes that has been the subject of more than a thousand publications. Genes for the symbiotic interaction with plants are well studied, but the adaptations that allow survival and growth in the soil environment are poorly understood. We have sequenced the genome of R. leguminosarum biovar viciae strain 3841. RESULTS: The 7.75 Mb genome comprises a circular chromosome and six circular plasmids, with 61% G+C overall. All three rRNA operons and 52 tRNA genes are on the chromosome; essential protein-encoding genes are largely chromosomal, but most functional classes occur on plasmids as well. Of the 7,263 protein-encoding genes, 2,056 had orthologs in each of three related genomes (Agrobacterium tumefaciens, Sinorhizobium meliloti, and Mesorhizobium loti), and these genes were over-represented in the chromosome and had above average G+C. Most supported the rRNA-based phylogeny, confirming A. tumefaciens to be the closest among these relatives, but 347 genes were incompatible with this phylogeny; these were scattered throughout the genome but were over-represented on the plasmids. An unexpectedly large number of genes were shared by all three rhizobia but were missing from A. tumefaciens. CONCLUSION: Overall, the genome can be considered to have two main components: a 'core', which is higher in G+C, is mostly chromosomal, is shared with related organisms, and has a consistent phylogeny; and an 'accessory' component, which is sporadic in distribution, lower in G+C, and located on the plasmids and chromosomal islands. The accessory genome has a different nucleotide composition from the core despite a long history of coexistence. Title: The genome of the African trypanosome Trypanosoma brucei Berriman M, Ghedin E, Hertz-Fowler C, Blandin G, Renauld H, Bartholomeu DC, Lennard NJ, Caler E, Hamlin NE and El-Sayed NM <92 more author(s)> Berriman M, Ghedin E, Hertz-Fowler C, Blandin G, Renauld H, Bartholomeu DC, Lennard NJ, Caler E, Hamlin NE, Haas B, Bohme U, Hannick L, Aslett MA, Shallom J, Marcello L, Hou L, Wickstead B, Alsmark UC, Arrowsmith C, Atkin RJ, Barron AJ, Bringaud F, Brooks K, Carrington M, Cherevach I, Chillingworth TJ, Churcher C, Clark LN, Corton CH, Cronin A, Davies RM, Doggett J, Djikeng A, Feldblyum T, Field MC, Fraser A, Goodhead I, Hance Z, Harper D, Harris BR, Hauser H, Hostetler J, Ivens A, Jagels K, Johnson D, Johnson J, Jones K, Kerhornou AX, Koo H, Larke N, Landfear S, Larkin C, Leech V, Line A, Lord A, MacLeod A, Mooney PJ, Moule S, Martin DM, Morgan GW, Mungall K, Norbertczak H, Ormond D, Pai G, Peacock CS, Peterson J, Quail MA, Rabbinowitsch E, Rajandream MA, Reitter C, Salzberg SL, Sanders M, Schobel S, Sharp S, Simmonds M, Simpson AJ, Tallon L, Turner CM, Tait A, Tivey AR, Van Aken S, Walker D, Wanless D, Wang S, White B, White O, Whitehead S, Woodward J, Wortman J, Adams MD, Embley TM, Gull K, Ullu E, Barry JD, Fairlamb AH, Opperdoes F, Barrell BG, Donelson JE, Hall N, Fraser CM, Melville SE, El-Sayed NM (- 92) Ref: Science, 309:416, 2005 : PubMed ESTHER: Berriman_2005_Science_309_416 PubMedSearch: Berriman 2005 Science 309 416 PubMedID: 16020726 Gene_locus related to this paper: tryb2-q6h9e3, tryb2-q6ha27, tryb2-q38cd5, tryb2-q38cd6, tryb2-q38cd7, tryb2-q38dc1, tryb2-q38de4, tryb2-q38ds6, tryb2-q38dx1, tryb2-q380z6, tryb2-q382c1, tryb2-q382l4, tryb2-q383a9, tryb2-q386e3, tryb2-q387r7, tryb2-q388n1, tryb2-q389w3, trybr-PEPTB, trycr-q4cq28, trycr-q4cq94, trycr-q4cq95, trycr-q4cq96, trycr-q4csm0, trycr-q4cwv3, trycr-q4cx66, trycr-q4cxr6, trycr-q4cyc5, trycr-q4cyf6, trycr-q4d3a2, trycr-q4d3x3, trycr-q4d3y4, trycr-q4d6h1, trycr-q4d8h8, trycr-q4d8h9, trycr-q4d8i0, trycr-q4d786, trycr-q4d975, trycr-q4da08, trycr-q4dap6, trycr-q4dbm2, trycr-q4dbn1, trycr-q4ddw7, trycr-q4de42, trycr-q4dhn8, trycr-q4dkk8, trycr-q4dkk9, trycr-q4dm56, trycr-q4dqa6, trycr-q4dt91, trycr-q4dvp2, trycr-q4dw34, trycr-q4dwm3, trycr-q4dy49, trycr-q4dy82, trycr-q4dzp6, trycr-q4e3m8, trycr-q4e4t5, trycr-q4e5d1, trycr-q4e5z2 Abstract 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. Title: The genome of the protist parasite Entamoeba histolytica Loftus B, Anderson I, Davies R, Alsmark UC, Samuelson J, Amedeo P, Roncaglia P, Berriman M, Hirt RP and Hall N <44 more author(s)> Loftus B, Anderson I, Davies R, Alsmark UC, Samuelson J, Amedeo P, Roncaglia P, Berriman M, Hirt RP, Mann BJ, Nozaki T, Suh B, Pop M, Duchene M, Ackers J, Tannich E, Leippe M, Hofer M, Bruchhaus I, Willhoeft U, Bhattacharya A, Chillingworth T, Churcher C, Hance Z, Harris B, Harris D, Jagels K, Moule S, Mungall K, Ormond D, Squares R, Whitehead S, Quail MA, Rabbinowitsch E, Norbertczak H, Price C, Wang Z, Guillen N, Gilchrist C, Stroup SE, Bhattacharya S, Lohia A, Foster PG, Sicheritz-Ponten T, Weber C, Singh U, Mukherjee C, El-Sayed NM, Petri WA, Jr., Clark CG, Embley TM, Barrell B, Fraser CM, Hall N (- 44) Ref: Nature, 433:865, 2005 : PubMed ESTHER: Loftus_2005_Nature_433_865 PubMedSearch: Loftus 2005 Nature 433 865 PubMedID: 15729342 Gene_locus related to this paper: entds-b0efg6, entds-b0egj2, enthi-b1n4x1, enthi-b1n449, enthi-b1n456, enthi-c4lsp4, enthi-c4lte6, enthi-c4lu03, enthi-c4lu54, enthi-c4lve4, enthi-c4lwe1, enthi-c4m0c3, enthi-c4m0e4, enthi-c4m1e7, enthi-c4m2a9, enthi-c4m2i4, enthi-c4m3r1, enthi-c4m4l3, enthi-c4m6g0, enthi-c4m6k3, enthi-c4m7k7, enthi-c4m7n4, enthi-c4m7v0, enthi-c4m8y5, enthi-c4m793, enthi-c4mb48, enthi-DPP, enthi-q50rh1, enthi-q50ya6, enthi-q51a37, enthi-q51aw6, enthi-q51ch3, enthi-q51cz6, enthi-q51ds3, enthi-q513q8, enthi-q513w3, enthi-q519v1 Abstract Entamoeba histolytica is an intestinal parasite and the causative agent of amoebiasis, which is a significant source of morbidity and mortality in developing countries. Here we present the genome of E. histolytica, which reveals a variety of metabolic adaptations shared with two other amitochondrial protist pathogens: Giardia lamblia and Trichomonas vaginalis. These adaptations include reduction or elimination of most mitochondrial metabolic pathways and the use of oxidative stress enzymes generally associated with anaerobic prokaryotes. Phylogenomic analysis identifies evidence for lateral gene transfer of bacterial genes into the E. histolytica genome, the effects of which centre on expanding aspects of E. histolytica's metabolic repertoire. The presence of these genes and the potential for novel metabolic pathways in E. histolytica may allow for the development of new chemotherapeutic agents. The genome encodes a large number of novel receptor kinases and contains expansions of a variety of gene families, including those associated with virulence. Additional genome features include an abundance of tandemly repeated transfer-RNA-containing arrays, which may have a structural function in the genome. Analysis of the genome provides new insights into the workings and genome evolution of a major human pathogen. Title: Genome sequence of the enterobacterial phytopathogen Erwinia carotovora subsp. atroseptica and characterization of virulence factors Bell KS, Sebaihia M, Pritchard L, Holden MT, Hyman LJ, Holeva MC, Thomson NR, Bentley SD, Churcher LJ and Toth IK <22 more author(s)> Bell KS, Sebaihia M, Pritchard L, Holden MT, Hyman LJ, Holeva MC, Thomson NR, Bentley SD, Churcher LJ, Mungall K, Atkin R, Bason N, Brooks K, Chillingworth T, Clark K, Doggett J, Fraser A, Hance Z, Hauser H, Jagels K, Moule S, Norbertczak H, Ormond D, Price C, Quail MA, Sanders M, Walker D, Whitehead S, Salmond GP, Birch PR, Parkhill J, Toth IK (- 22) Ref: Proc Natl Acad Sci U S A, 101:11105, 2004 : PubMed ESTHER: Bell_2004_Proc.Natl.Acad.Sci.U.S.A_101_11105 PubMedSearch: Bell 2004 Proc.Natl.Acad.Sci.U.S.A 101 11105 PubMedID: 15263089 Gene_locus related to this paper: erwct-q6czi2, erwct-q6czl9, erwct-q6czu1, erwct-q6d0l3, erwct-q6d1e3, erwct-q6d1l9, erwct-q6d2k4, erwct-q6d2x2, erwct-q6d3m9, erwct-q6d4b7, erwct-q6d6t8, erwct-q6d7j1, erwct-q6d7p5, erwct-q6d7w3, erwct-q6d8k2, erwct-q6d8q7, erwct-q6d9l2, erwct-q6d041, erwct-q6d134, erwct-q6d207, erwct-q6d508, erwct-q6d615, erwct-q6d673, erwct-q6d739.1, erwct-q6d739.2, erwct-q6d884, erwct-q6da42, erwct-q6da66, erwct-q6dac1, erwct-q6dar9, erwct-Y3465 Abstract The bacterial family Enterobacteriaceae is notable for its well studied human pathogens, including Salmonella, Yersinia, Shigella, and Escherichia spp. However, it also contains several plant pathogens. We report the genome sequence of a plant pathogenic enterobacterium, Erwinia carotovora subsp. atroseptica (Eca) strain SCRI1043, the causative agent of soft rot and blackleg potato diseases. Approximately 33% of Eca genes are not shared with sequenced enterobacterial human pathogens, including some predicted to facilitate unexpected metabolic traits, such as nitrogen fixation and opine catabolism. This proportion of genes also contains an overrepresentation of pathogenicity determinants, including possible horizontally acquired gene clusters for putative type IV secretion and polyketide phytotoxin synthesis. To investigate whether these gene clusters play a role in the disease process, an arrayed set of insertional mutants was generated, and mutations were identified. Plant bioassays showed that these mutants were significantly reduced in virulence, demonstrating both the presence of novel pathogenicity determinants in Eca, and the impact of functional genomics in expanding our understanding of phytopathogenicity in the Enterobacteriaceae. Title: Complete genomes of two clinical Staphylococcus aureus strains: evidence for the rapid evolution of virulence and drug resistance Holden MT, Feil EJ, Lindsay JA, Peacock SJ, Day NP, Enright MC, Foster TJ, Moore CE, Hurst L and Parkhill J <35 more author(s)> Holden MT, Feil EJ, Lindsay JA, Peacock SJ, Day NP, Enright MC, Foster TJ, Moore CE, Hurst L, Atkin R, Barron A, Bason N, Bentley SD, Chillingworth C, Chillingworth T, Churcher C, Clark L, Corton C, Cronin A, Doggett J, Dowd L, Feltwell T, Hance Z, Harris B, Hauser H, Holroyd S, Jagels K, James KD, Lennard N, Line A, Mayes R, Moule S, Mungall K, Ormond D, Quail MA, Rabbinowitsch E, Rutherford K, Sanders M, Sharp S, Simmonds M, Stevens K, Whitehead S, Barrell BG, Spratt BG, Parkhill J (- 35) Ref: Proc Natl Acad Sci U S A, 101:9786, 2004 : PubMed ESTHER: Holden_2004_Proc.Natl.Acad.Sci.U.S.A_101_9786 PubMedSearch: Holden 2004 Proc.Natl.Acad.Sci.U.S.A 101 9786 PubMedID: 15213324 Gene_locus related to this paper: staau-d2feb3, staau-d2uin3, staau-LIP, staau-lipas, staau-MW0741, staau-MW2456, staau-q6gfm6, staau-SA0011, staau-SA0569, staau-SA0572, staau-SA0897, staau-SA1143, staau-SA2240, staau-SA2306, staau-SA2367, staau-SA2422, staau-SAV0321, staau-SAV0446, staau-SAV0457, staau-SAV0655, staau-SAV1014, staau-SAV1765, staau-SAV1793, staau-SAV2188, staau-SAV2350, staau-SAV2594 Abstract Staphylococcus aureus is an important nosocomial and community-acquired pathogen. Its genetic plasticity has facilitated the evolution of many virulent and drug-resistant strains, presenting a major and constantly changing clinical challenge. We sequenced the approximately 2.8-Mbp genomes of two disease-causing S. aureus strains isolated from distinct clinical settings: a recent hospital-acquired representative of the epidemic methicillin-resistant S. aureus EMRSA-16 clone (MRSA252), a clinically important and globally prevalent lineage; and a representative of an invasive community-acquired methicillin-susceptible S. aureus clone (MSSA476). A comparative-genomics approach was used to explore the mechanisms of evolution of clinically important S. aureus genomes and to identify regions affecting virulence and drug resistance. The genome sequences of MRSA252 and MSSA476 have a well conserved core region but differ markedly in their accessory genetic elements. MRSA252 is the most genetically diverse S. aureus strain sequenced to date: approximately 6% of the genome is novel compared with other published genomes, and it contains several unique genetic elements. MSSA476 is methicillin-susceptible, but it contains a novel Staphylococcal chromosomal cassette (SCC) mec-like element (designated SCC(476)), which is integrated at the same site on the chromosome as SCCmec elements in MRSA strains but encodes a putative fusidic acid resistance protein. The crucial role that accessory elements play in the rapid evolution of S. aureus is clearly illustrated by comparing the MSSA476 genome with that of an extremely closely related MRSA community-acquired strain; the differential distribution of large mobile elements carrying virulence and drug-resistance determinants may be responsible for the clinically important phenotypic differences in these strains. Title: Genomic plasticity of the causative agent of melioidosis, Burkholderia pseudomallei Holden MT, Titball RW, Peacock SJ, Cerdeno-Tarraga AM, Atkins T, Crossman LC, Pitt T, Churcher C, Mungall K and Parkhill J <38 more author(s)> Holden MT, Titball RW, Peacock SJ, Cerdeno-Tarraga AM, Atkins T, Crossman LC, Pitt T, Churcher C, Mungall K, Bentley SD, Sebaihia M, Thomson NR, Bason N, Beacham IR, Brooks K, Brown KA, Brown NF, Challis GL, Cherevach I, Chillingworth T, Cronin A, Crossett B, Davis P, DeShazer D, Feltwell T, Fraser A, Hance Z, Hauser H, Holroyd S, Jagels K, Keith KE, Maddison M, Moule S, Price C, Quail MA, Rabbinowitsch E, Rutherford K, Sanders M, Simmonds M, Songsivilai S, Stevens K, Tumapa S, Vesaratchavest M, Whitehead S, Yeats C, Barrell BG, Oyston PC, Parkhill J (- 38) Ref: Proc Natl Acad Sci U S A, 101:14240, 2004 : PubMed ESTHER: Holden_2004_Proc.Natl.Acad.Sci.U.S.A_101_14240 PubMedSearch: Holden 2004 Proc.Natl.Acad.Sci.U.S.A 101 14240 PubMedID: 15377794 Gene_locus related to this paper: burma-a5j5w8, burma-a5tj72, burma-a5tq93, burma-metx, burma-q62a61, burma-q62ar2.1, burma-q62ar2.2, burma-q62ax8, burma-q62b60, burma-q62b79, burma-q62bh9, burma-q62bl4, burma-q62bl7, burma-q62c00, burma-q62cg5, burma-q62d41, burma-q62d56, burma-q62d83, burma-q62dg2, burma-q62du7, burma-q62e67, burma-q62eb8, burma-q62ed8, burma-q62f28, burma-q62fx7, burma-q62g26, burma-q62gx9, burma-q62gy2, burma-q62hq2, burma-q62i62, burma-q62ib8, burma-q62ie8, burma-q62j07, burma-q62j15, burma-q62jn5, burma-q62jy7, burma-q62kb7, burma-q62kg0, burma-q62kh9, burma-q62lp7, burma-q62m40, burma-q62mc3, burma-q62mf4, burma-q62mq7, burma-q629m1, burma-q629p4, burma-q629u0, burp1-q3jvq2, burps-a4lm41, burps-q3v7s4, burps-q63hx2, burps-q63i95, burps-q63im5, burps-q63is4, burps-q63ja6, burps-q63ja9, burps-q63jh5, burps-q63l17, burps-q63l41, burps-q63l44, burps-q63lt9, burps-q63me1, burps-q63mj7, burps-q63mj8, burps-q63mn8, burps-q63mr2, burps-q63n52, burps-q63p18, burps-q63p99, burps-q63ug2, burps-q63ug5, burps-q63xf9, burps-q63y36, burps-q63y45, burps-q63y52, burps-q63y59, burta-q2t474, burps-hboh Abstract Burkholderia pseudomallei is a recognized biothreat agent and the causative agent of melioidosis. This Gram-negative bacterium exists as a soil saprophyte in melioidosis-endemic areas of the world and accounts for 20% of community-acquired septicaemias in northeastern Thailand where half of those affected die. Here we report the complete genome of B. pseudomallei, which is composed of two chromosomes of 4.07 megabase pairs and 3.17 megabase pairs, showing significant functional partitioning of genes between them. The large chromosome encodes many of the core functions associated with central metabolism and cell growth, whereas the small chromosome carries more accessory functions associated with adaptation and survival in different niches. Genomic comparisons with closely and more distantly related bacteria revealed a greater level of gene order conservation and a greater number of orthologous genes on the large chromosome, suggesting that the two replicons have distinct evolutionary origins. A striking feature of the genome was the presence of 16 genomic islands (GIs) that together made up 6.1% of the genome. Further analysis revealed these islands to be variably present in a collection of invasive and soil isolates but entirely absent from the clonally related organism B. mallei. We propose that variable horizontal gene acquisition by B. pseudomallei is an important feature of recent genetic evolution and that this has resulted in a genetically diverse pathogenic species. Title: The complete genome sequence and analysis of Corynebacterium diphtheriae NCTC13129 Cerdeno-Tarraga AM, Efstratiou A, Dover LG, Holden MT, Pallen M, Bentley SD, Besra GS, Churcher C, James KD and Parkhill J <16 more author(s)> Cerdeno-Tarraga AM, Efstratiou A, Dover LG, Holden MT, Pallen M, Bentley SD, Besra GS, Churcher C, James KD, De Zoysa A, Chillingworth T, Cronin A, Dowd L, Feltwell T, Hamlin N, Holroyd S, Jagels K, Moule S, Quail MA, Rabbinowitsch E, Rutherford KM, Thomson NR, Unwin L, Whitehead S, Barrell BG, Parkhill J (- 16) Ref: Nucleic Acids Research, 31:6516, 2003 : PubMed ESTHER: Cerdeno-Tarraga_2003_Nucleic.Acids.Res_31_6516 PubMedSearch: Cerdeno-Tarraga 2003 Nucleic.Acids.Res 31 6516 PubMedID: 14602910 Gene_locus related to this paper: cordi-DIP1007, cordi-DIP1729, cordi-q6ned6, cordi-q6nes3, cordi-q6nes4, cordi-q6nes6, cordi-q6nes8, cordi-q6nev5, cordi-q6nex0, cordi-q6nez6, cordi-q6nf79, cordi-q6nfa8, cordi-q6nfg5, cordi-q6nfz1, cordi-q6ng42, cordi-q6ngl8, cordi-q6nhd8, cordi-q6niz3, cordi-q6nj46, cordi-q6njn3, cordi-q6njn4, cordi-q6njt5, cordi-q6nkb6, cordk-h2hkn5 Abstract Corynebacterium diphtheriae is a Gram-positive, non-spore forming, non-motile, pleomorphic rod belonging to the genus Corynebacterium and the actinomycete group of organisms. The organism produces a potent bacteriophage-encoded protein exotoxin, diphtheria toxin (DT), which causes the symptoms of diphtheria. This potentially fatal infectious disease is controlled in many developed countries by an effective immunisation programme. However, the disease has made a dramatic return in recent years, in particular within the Eastern European region. The largest, and still on-going, outbreak since the advent of mass immunisation started within Russia and the newly independent states of the former Soviet Union in the 1990s. We have sequenced the genome of a UK clinical isolate (biotype gravis strain NCTC13129), representative of the clone responsible for this outbreak. The genome consists of a single circular chromosome of 2 488 635 bp, with no plasmids. It provides evidence that recent acquisition of pathogenicity factors goes beyond the toxin itself, and includes iron-uptake systems, adhesins and fimbrial proteins. This is in contrast to Corynebacterium's nearest sequenced pathogenic relative, Mycobacterium tuberculosis, where there is little evidence of recent horizontal DNA acquisition. The genome itself shows an unusually extreme large-scale compositional bias, being noticeably higher in G+C near the origin than at the terminus. Title: Comparative analysis of the genome sequences of Bordetella pertussis, Bordetella parapertussis and Bordetella bronchiseptica Parkhill J, Sebaihia M, Preston A, Murphy LD, Thomson N, Harris DE, Holden MT, Churcher CM, Bentley SD and Maskell DJ <43 more author(s)> Parkhill J, Sebaihia M, Preston A, Murphy LD, Thomson N, Harris DE, Holden MT, Churcher CM, Bentley SD, Mungall KL, Cerdeno-Tarraga AM, Temple L, James K, Harris B, Quail MA, Achtman M, Atkin R, Baker S, Basham D, Bason N, Cherevach I, Chillingworth T, Collins M, Cronin A, Davis P, Doggett J, Feltwell T, Goble A, Hamlin N, Hauser H, Holroyd S, Jagels K, Leather S, Moule S, Norberczak H, O'Neil S, Ormond D, Price C, Rabbinowitsch E, Rutter S, Sanders M, Saunders D, Seeger K, Sharp S, Simmonds M, Skelton J, Squares R, Squares S, Stevens K, Unwin L, Whitehead S, Barrell BG, Maskell DJ (- 43) Ref: Nat Genet, 35:32, 2003 : PubMed ESTHER: Parkhill_2003_Nat.Genet_35_32 PubMedSearch: Parkhill 2003 Nat.Genet 35 32 PubMedID: 12910271 Gene_locus related to this paper: borbr-BB0273, borbr-BB0570, borbr-BB0670, borbr-BB1064, borbr-BB1079, borbr-BB1247, borbr-BB1498, borbr-BB2718, borbr-BB4129, borbr-BB4247, borbr-MHPC, borbr-q7wdw1, borbr-q7wiz8, borbr-q7wk25, borbr-q7wmc2, borbr-q7wpd9, borpa-q7w3f3, borpa-q7w9v8, borpe-BIOH, borpe-BP0300, borpe-BP2114, borpe-BP2146, borpe-BP2511, borpe-BP3096, borpe-BP3623, borpe-BP3691, borpe-CATD2, borpe-METX, borpe-O30449, borpe-PHBC, borpe-q7vsl4, borpe-q7vt07, borpe-q7vtg0, borpe-q7vtv2, borpe-q7vus4, borpe-q7vuv4, borpe-q7vv11, borpe-q7vv48, borpe-q7vvf6, borpe-q7vwu4, borpe-q7vyn0, borpe-q7vyq4, borpe-q7vz26, borpe-q7vzb4, borpe-q7vzj6, borpe-q7w073 Abstract Bordetella pertussis, Bordetella parapertussis and Bordetella bronchiseptica are closely related Gram-negative beta-proteobacteria that colonize the respiratory tracts of mammals. B. pertussis is a strict human pathogen of recent evolutionary origin and is the primary etiologic agent of whooping cough. B. parapertussis can also cause whooping cough, and B. bronchiseptica causes chronic respiratory infections in a wide range of animals. We sequenced the genomes of B. bronchiseptica RB50 (5,338,400 bp; 5,007 predicted genes), B. parapertussis 12822 (4,773,551 bp; 4,404 genes) and B. pertussis Tohama I (4,086,186 bp; 3,816 genes). Our analysis indicates that B. parapertussis and B. pertussis are independent derivatives of B. bronchiseptica-like ancestors. During the evolution of these two host-restricted species there was large-scale gene loss and inactivation; host adaptation seems to be a consequence of loss, not gain, of function, and differences in virulence may be related to loss of regulatory or control functions. Title: Sequence of Plasmodium falciparum chromosomes 1, 3-9 and 13 Hall N, Pain A, Berriman M, Churcher C, Harris B, Harris D, Mungall K, Bowman S, Atkin R and Barrell BG <70 more author(s)> Hall N, Pain A, Berriman M, Churcher C, Harris B, Harris D, Mungall K, Bowman S, Atkin R, Baker S, Barron A, Brooks K, Buckee CO, Burrows C, Cherevach I, Chillingworth C, Chillingworth T, Christodoulou Z, Clark L, Clark R, Corton C, Cronin A, Davies R, Davis P, Dear P, Dearden F, Doggett J, Feltwell T, Goble A, Goodhead I, Gwilliam R, Hamlin N, Hance Z, Harper D, Hauser H, Hornsby T, Holroyd S, Horrocks P, Humphray S, Jagels K, James KD, Johnson D, Kerhornou A, Knights A, Konfortov B, Kyes S, Larke N, Lawson D, Lennard N, Line A, Maddison M, McLean J, Mooney P, Moule S, Murphy L, Oliver K, Ormond D, Price C, Quail MA, Rabbinowitsch E, Rajandream MA, Rutter S, Rutherford KM, Sanders M, Simmonds M, Seeger K, Sharp S, Smith R, Squares R, Squares S, Stevens K, Taylor K, Tivey A, Unwin L, Whitehead S, Woodward J, Sulston JE, Craig A, Newbold C, Barrell BG (- 70) Ref: Nature, 419:527, 2002 : PubMed ESTHER: Hall_2002_Nature_419_527 PubMedSearch: Hall 2002 Nature 419 527 PubMedID: 12368867 Gene_locus related to this paper: plaf7-c0h4q4, plafa-MAL6P1.135, plafa-PFD0185C, plafa-PFI1775W, plafa-PFI1800W Abstract Since the sequencing of the first two chromosomes of the malaria parasite, Plasmodium falciparum, there has been a concerted effort to sequence and assemble the entire genome of this organism. Here we report the sequence of chromosomes 1, 3-9 and 13 of P. falciparum clone 3D7--these chromosomes account for approximately 55% of the total genome. We describe the methods used to map, sequence and annotate these chromosomes. By comparing our assemblies with the optical map, we indicate the completeness of the resulting sequence. During annotation, we assign Gene Ontology terms to the predicted gene products, and observe clustering of some malaria-specific terms to specific chromosomes. We identify a highly conserved sequence element found in the intergenic region of internal var genes that is not associated with their telomeric counterparts. Title: The genome sequence of Schizosaccharomyces pombe Wood V, Gwilliam R, Rajandream MA, Lyne M, Lyne R, Stewart A, Sgouros J, Peat N, Hayles J and Nurse P <124 more author(s)> Wood V, Gwilliam R, Rajandream MA, Lyne M, Lyne R, Stewart A, Sgouros J, Peat N, Hayles J, Baker S, Basham D, Bowman S, Brooks K, Brown D, Brown S, Chillingworth T, Churcher C, Collins M, Connor R, Cronin A, Davis P, Feltwell T, Fraser A, Gentles S, Goble A, Hamlin N, Harris D, Hidalgo J, Hodgson G, Holroyd S, Hornsby T, Howarth S, Huckle EJ, Hunt S, Jagels K, James K, Jones L, Jones M, Leather S, McDonald S, McLean J, Mooney P, Moule S, Mungall K, Murphy L, Niblett D, Odell C, Oliver K, O'Neil S, Pearson D, Quail MA, Rabbinowitsch E, Rutherford K, Rutter S, Saunders D, Seeger K, Sharp S, Skelton J, Simmonds M, Squares R, Squares S, Stevens K, Taylor K, Taylor RG, Tivey A, Walsh S, Warren T, Whitehead S, Woodward J, Volckaert G, Aert R, Robben J, Grymonprez B, Weltjens I, Vanstreels E, Rieger M, Schafer M, Muller-Auer S, Gabel C, Fuchs M, Dusterhoft A, Fritzc C, Holzer E, Moestl D, Hilbert H, Borzym K, Langer I, Beck A, Lehrach H, Reinhardt R, Pohl TM, Eger P, Zimmermann W, Wedler H, Wambutt R, Purnelle B, Goffeau A, Cadieu E, Dreano S, Gloux S, Lelaure V, Mottier S, Galibert F, Aves SJ, Xiang Z, Hunt C, Moore K, Hurst SM, Lucas M, Rochet M, Gaillardin C, Tallada VA, Garzon A, Thode G, Daga RR, Cruzado L, Jimenez J, Sanchez M, del Rey F, Benito J, Dominguez A, Revuelta JL, Moreno S, Armstrong J, Forsburg SL, Cerutti L, Lowe T, McCombie WR, Paulsen I, Potashkin J, Shpakovski GV, Ussery D, Barrell BG, Nurse P (- 124) Ref: Nature, 415:871, 2002 : PubMed ESTHER: Wood_2002_Nature_415_871 PubMedSearch: Wood 2002 Nature 415 871 PubMedID: 11859360 Gene_locus related to this paper: schpo-APTH1, schpo-be46, schpo-BST1, schpo-C2E11.08, schpo-C14C4.15C, schpo-C22H12.03, schpo-C23C4.16C, schpo-C57A10.08C, schpo-dyr, schpo-este1, schpo-KEX1, schpo-PCY1, schpo-pdat, schpo-PLG7, schpo-ppme1, schpo-q9c0y8, schpo-SPAC4A8.06C, schpo-C22A12.06C, schpo-SPAC977.15, schpo-SPAPB1A11.02, schpo-SPBC14C8.15, schpo-SPBC530.12C, schpo-SPBC1711.12, schpo-SPBPB2B2.02, schpo-SPCC5E4.05C, schpo-SPCC417.12, schpo-SPCC1672.09, schpo-yb4e, schpo-yblh, schpo-ydw6, schpo-ye7a, schpo-ye63, schpo-ye88, schpo-yeld, schpo-yk68, schpo-clr3, schpo-ykv6 Abstract We have sequenced and annotated the genome of fission yeast (Schizosaccharomyces pombe), which contains the smallest number of protein-coding genes yet recorded for a eukaryote: 4,824. The centromeres are between 35 and 110 kilobases (kb) and contain related repeats including a highly conserved 1.8-kb element. Regions upstream of genes are longer than in budding yeast (Saccharomyces cerevisiae), possibly reflecting more-extended control regions. Some 43% of the genes contain introns, of which there are 4,730. Fifty genes have significant similarity with human disease genes; half of these are cancer related. We identify highly conserved genes important for eukaryotic cell organization including those required for the cytoskeleton, compartmentation, cell-cycle control, proteolysis, protein phosphorylation and RNA splicing. These genes may have originated with the appearance of eukaryotic life. Few similarly conserved genes that are important for multicellular organization were identified, suggesting that the transition from prokaryotes to eukaryotes required more new genes than did the transition from unicellular to multicellular organization. Title: Massive gene decay in the leprosy bacillus Cole ST, Eiglmeier K, Parkhill J, James KD, Thomson NR, Wheeler PR, Honore N, Garnier T, Churcher C and Barrell BG <34 more author(s)> Cole ST, Eiglmeier K, Parkhill J, James KD, Thomson NR, Wheeler PR, Honore N, Garnier T, Churcher C, Harris D, Mungall K, Basham D, Brown D, Chillingworth T, Connor R, Davies RM, Devlin K, Duthoy S, Feltwell T, Fraser A, Hamlin N, Holroyd S, Hornsby T, Jagels K, Lacroix C, Maclean J, Moule S, Murphy L, Oliver K, Quail MA, Rajandream MA, Rutherford KM, Rutter S, Seeger K, Simon S, Simmonds M, Skelton J, Squares R, Squares S, Stevens K, Taylor K, Whitehead S, Woodward JR, Barrell BG (- 34) Ref: Nature, 409:1007, 2001 : PubMed ESTHER: Cole_2001_Nature_409_1007 PubMedSearch: Cole 2001 Nature 409 1007 PubMedID: 11234002 Gene_locus related to this paper: mycle-a85a, mycle-a85b, mycle-a85c, mycle-lipG, mycle-LPQC, mycle-metx, mycle-ML0314, mycle-ML0370, mycle-ML0376, mycle-ML1339, mycle-ML1444, mycle-ML1632, mycle-ML1633, mycle-ML1921, mycle-ML2269, mycle-ML2297, mycle-ML2359, mycle-ML2603, mycle-mpt5, mycle-PKS13, mycle-PTRB, mycle-q9cc62, mycle-q9cdb3 Abstract Leprosy, a chronic human neurological disease, results from infection with the obligate intracellular pathogen Mycobacterium leprae, a close relative of the tubercle bacillus. Mycobacterium leprae has the longest doubling time of all known bacteria and has thwarted every effort at culture in the laboratory. Comparing the 3.27-megabase (Mb) genome sequence of an armadillo-derived Indian isolate of the leprosy bacillus with that of Mycobacterium tuberculosis (4.41 Mb) provides clear explanations for these properties and reveals an extreme case of reductive evolution. Less than half of the genome contains functional genes but pseudogenes, with intact counterparts in M. tuberculosis, abound. Genome downsizing and the current mosaic arrangement appear to have resulted from extensive recombination events between dispersed repetitive sequences. Gene deletion and decay have eliminated many important metabolic activities including siderophore production, part of the oxidative and most of the microaerophilic and anaerobic respiratory chains, and numerous catabolic systems and their regulatory circuits. Title: Genome sequence of Yersinia pestis, the causative agent of plague. Parkhill J, Wren BW, Thomson NR, Titball RW, Holden MTG, Prentice MB, Sebaihia M, James KD, Churcher C and Barrell BG <25 more author(s)> Parkhill J, Wren BW, Thomson NR, Titball RW, Holden MTG, Prentice MB, Sebaihia M, James KD, Churcher C, Mungall KL, Baker S, Basham D, Bentley SD, Brooks K, Cerdeno-Tarraga AM, Chillingworth T, Cronin A, Davies RM, Davis P, Dougan G, Feltwell T, Hamlin N, Holroyd S, Jagels K, Karlyshev AV, Leather S, Moule S, Oyston PCF, Quail M, Rutherford K, Simmonds M, Skelton J, Stevens K, Whitehead S, Barrell BG (- 25) Ref: Nature, 413:523, 2001 : PubMed ESTHER: Parkhill_2001_Nature_413_523 PubMedSearch: Parkhill 2001 Nature 413 523 PubMedID: 11586360 Gene_locus related to this paper: yerpe-BIOH, yerpe-dlhh, yerpe-IRP1, yerpe-PIP, yerpe-PLDB, yerpe-PTRB, yerpe-q8zey9, yerpe-y1616, yerpe-y3224, yerpe-YBTT, yerpe-YPLA, yerpe-YPO0180, yerpe-YPO0667, yerpe-YPO0773, yerpe-YPO0776, yerpe-YPO0986, yerpe-YPO1501, yerpe-YPO1997, yerpe-YPO2002, yerpe-YPO2336, yerpe-YPO2526, yerpe-YPO2638, yerpe-YPO2814, yerpe-YPO4014 Abstract The Gram-negative bacterium Yersinia pestis is the causative agent of the systemic invasive infectious disease classically referred to as plague, and has been responsible for three human pandemics: the Justinian plague (sixth to eighth centuries), the Black Death (fourteenth to nineteenth centuries) and modern plague (nineteenth century to the present day). The recent identification of strains resistant to multiple drugs and the potential use of Y. pestis as an agent of biological warfare mean that plague still poses a threat to human health. Here we report the complete genome sequence of Y. pestis strain CO92, consisting of a 4.65-megabase (Mb) chromosome and three plasmids of 96.2 kilobases (kb), 70.3 kb and 9.6 kb. The genome is unusually rich in insertion sequences and displays anomalies in GC base-composition bias, indicating frequent intragenomic recombination. Many genes seem to have been acquired from other bacteria and viruses (including adhesins, secretion systems and insecticidal toxins). The genome contains around 150 pseudogenes, many of which are remnants of a redundant enteropathogenic lifestyle. The evidence of ongoing genome fluidity, expansion and decay suggests Y. pestis is a pathogen that has undergone large-scale genetic flux and provides a unique insight into the ways in which new and highly virulent pathogens evolve. Title: Complete genome sequence of a multiple drug resistant Salmonella enterica serovar Typhi CT18 Parkhill J, Dougan G, James KD, Thomson NR, Pickard D, Wain J, Churcher C, Mungall KL, Bentley SD and Barrell BG <31 more author(s)> Parkhill J, Dougan G, James KD, Thomson NR, Pickard D, Wain J, Churcher C, Mungall KL, Bentley SD, Holden MT, Sebaihia M, Baker S, Basham D, Brooks K, Chillingworth T, Connerton P, Cronin A, Davis P, Davies RM, Dowd L, White N, Farrar J, Feltwell T, Hamlin N, Haque A, Hien TT, Holroyd S, Jagels K, Krogh A, Larsen TS, Leather S, Moule S, O'Gaora P, Parry C, Quail M, Rutherford K, Simmonds M, Skelton J, Stevens K, Whitehead S, Barrell BG (- 31) Ref: Nature, 413:848, 2001 : PubMed ESTHER: Parkhill_2001_Nature_413_848 PubMedSearch: Parkhill 2001 Nature 413 848 PubMedID: 11677608 Gene_locus related to this paper: salen-OPDB, salti-q8z717, salty-AES, salty-BIOH, salty-ENTF, salty-FES, salty-IROD, salty-IROE, salty-PLDB, salty-STM2547, salty-STM4506, salty-STY1441, salty-STY2428, salty-STY3846, salty-yafa, salty-YBFF, salty-ycfp, salty-YFBB, salty-YJFP, salty-YQIA Abstract Salmonella enterica serovar Typhi (S. typhi) is the aetiological agent of typhoid fever, a serious invasive bacterial disease of humans with an annual global burden of approximately 16 million cases, leading to 600,000 fatalities. Many S. enterica serovars actively invade the mucosal surface of the intestine but are normally contained in healthy individuals by the local immune defence mechanisms. However, S. typhi has evolved the ability to spread to the deeper tissues of humans, including liver, spleen and bone marrow. Here we have sequenced the 4,809,037-base pair (bp) genome of a S. typhi (CT18) that is resistant to multiple drugs, revealing the presence of hundreds of insertions and deletions compared with the Escherichia coli genome, ranging in size from single genes to large islands. Notably, the genome sequence identifies over two hundred pseudogenes, several corresponding to genes that are known to contribute to virulence in Salmonella typhimurium. This genetic degradation may contribute to the human-restricted host range for S. typhi. CT18 harbours a 218,150-bp multiple-drug-resistance incH1 plasmid (pHCM1), and a 106,516-bp cryptic plasmid (pHCM2), which shows recent common ancestry with a virulence plasmid of Yersinia pestis. Title: Complete DNA sequence of a serogroup A strain of Neisseria meningitidis Z2491 Parkhill J, Achtman M, James KD, Bentley SD, Churcher C, Klee SR, Morelli G, Basham D, Brown D and Barrell BG <18 more author(s)> Parkhill J, Achtman M, James KD, Bentley SD, Churcher C, Klee SR, Morelli G, Basham D, Brown D, Chillingworth T, Davies RM, Davis P, Devlin K, Feltwell T, Hamlin N, Holroyd S, Jagels K, Leather S, Moule S, Mungall K, Quail MA, Rajandream MA, Rutherford KM, Simmonds M, Skelton J, Whitehead S, Spratt BG, Barrell BG (- 18) Ref: Nature, 404:502, 2000 : PubMed ESTHER: Parkhill_2000_Nature_404_502 PubMedSearch: Parkhill 2000 Nature 404 502 PubMedID: 10761919 Gene_locus related to this paper: neima-metx, neimb-q9k0t9, neime-ESD, neime-NMA2216, neime-NMB0276, neime-NMB1877, neimf-a1kta9, neime-r0tza2 Abstract Neisseria meningitidis causes bacterial meningitis and is therefore responsible for considerable morbidity and mortality in both the developed and the developing world. Meningococci are opportunistic pathogens that colonize the nasopharynges and oropharynges of asymptomatic carriers. For reasons that are still mostly unknown, they occasionally gain access to the blood, and subsequently to the cerebrospinal fluid, to cause septicaemia and meningitis. N. meningitidis strains are divided into a number of serogroups on the basis of the immunochemistry of their capsular polysaccharides; serogroup A strains are responsible for major epidemics and pandemics of meningococcal disease, and therefore most of the morbidity and mortality associated with this disease. Here we have determined the complete genome sequence of a serogroup A strain of Neisseria meningitidis, Z2491. The sequence is 2,184,406 base pairs in length, with an overall G+C content of 51.8%, and contains 2,121 predicted coding sequences. The most notable feature of the genome is the presence of many hundreds of repetitive elements, ranging from short repeats, positioned either singly or in large multiple arrays, to insertion sequences and gene duplications of one kilobase or more. Many of these repeats appear to be involved in genome fluidity and antigenic variation in this important human pathogen. Title: The genome sequence of the food-borne pathogen Campylobacter jejuni reveals hypervariable sequences Parkhill J, Wren BW, Mungall K, Ketley JM, Churcher C, Basham D, Chillingworth T, Davies RM, Feltwell T and Barrell BG <11 more author(s)> Parkhill J, Wren BW, Mungall K, Ketley JM, Churcher C, Basham D, Chillingworth T, Davies RM, Feltwell T, Holroyd S, Jagels K, Karlyshev AV, Moule S, Pallen MJ, Penn CW, Quail MA, Rajandream MA, Rutherford KM, van Vliet AH, Whitehead S, Barrell BG (- 11) Ref: Nature, 403:665, 2000 : PubMed ESTHER: Parkhill_2000_Nature_403_665 PubMedSearch: Parkhill 2000 Nature 403 665 PubMedID: 10688204 Gene_locus related to this paper: camco-e0qbj3, camco-q4hhu5, camje-a3zji1, camje-CJ0796C, camjr-q5ht69, camju-a3yll6, camju-Q9ZF63 Abstract Campylobacter jejuni, from the delta-epsilon group of proteobacteria, is a microaerophilic, Gram-negative, flagellate, spiral bacterium-properties it shares with the related gastric pathogen Helicobacter pylori. It is the leading cause of bacterial food-borne diarrhoeal disease throughout the world. In addition, infection with C. jejuni is the most frequent antecedent to a form of neuromuscular paralysis known as Guillain-Barre syndrome. Here we report the genome sequence of C. jejuni NCTC11168. C. jejuni has a circular chromosome of 1,641,481 base pairs (30.6% G+C) which is predicted to encode 1,654 proteins and 54 stable RNA species. The genome is unusual in that there are virtually no insertion sequences or phage-associated sequences and very few repeat sequences. One of the most striking findings in the genome was the presence of hypervariable sequences. These short homopolymeric runs of nucleotides were commonly found in genes encoding the biosynthesis or modification of surface structures, or in closely linked genes of unknown function. The apparently high rate of variation of these homopolymeric tracts may be important in the survival strategy of C. jejuni. Title: The complete nucleotide sequence of chromosome 3 of Plasmodium falciparum Bowman S, Lawson D, Basham D, Brown D, Chillingworth T, Churcher CM, Craig A, Davies RM, Devlin K and Barrell BG <26 more author(s)> Bowman S, Lawson D, Basham D, Brown D, Chillingworth T, Churcher CM, Craig A, Davies RM, Devlin K, Feltwell T, Gentles S, Gwilliam R, Hamlin N, Harris D, Holroyd S, Hornsby T, Horrocks P, Jagels K, Jassal B, Kyes S, McLean J, Moule S, Mungall K, Murphy L, Oliver K, Quail MA, Rajandream MA, Rutter S, Skelton J, Squares R, Squares S, Sulston JE, Whitehead S, Woodward JR, Newbold C, Barrell BG (- 26) Ref: Nature, 400:532, 1999 : PubMed ESTHER: Bowman_1999_Nature_400_532 PubMedSearch: Bowman 1999 Nature 400 532 PubMedID: 10448855 Gene_locus related to this paper: plafa-PFC0950C Abstract Analysis of Plasmodium falciparum chromosome 3, and comparison with chromosome 2, highlights novel features of chromosome organization and gene structure. The sub-telomeric regions of chromosome 3 show a conserved order of features, including repetitive DNA sequences, members of multigene families involved in pathogenesis and antigenic variation, a number of conserved pseudogenes, and several genes of unknown function. A putative centromere has been identified that has a core region of about 2 kilobases with an extremely high (adenine + thymidine) composition and arrays of tandem repeats. We have predicted 215 protein-coding genes and two transfer RNA genes in the 1,060,106-base-pair chromosome sequence. The predicted protein-coding genes can be divided into three main classes: 52.6% are not spliced, 45.1% have a large exon with short additional 5' or 3' exons, and 2.3% have a multiple exon structure more typical of higher eukaryotes. Title: Deciphering the biology of Mycobacterium tuberculosis from the complete genome sequence Cole ST, Brosch R, Parkhill J, Garnier T, Churcher C, Harris D, Gordon SV, Eiglmeier K, Gas S and Barrell BG <32 more author(s)> Cole ST, Brosch R, Parkhill J, Garnier T, Churcher C, Harris D, Gordon SV, Eiglmeier K, Gas S, Barry CE, 3rd, Tekaia F, Badcock K, Basham D, Brown D, Chillingworth T, Connor R, Davies R, Devlin K, Feltwell T, Gentles S, Hamlin N, Holroyd S, Hornsby T, Jagels K, Krogh A, McLean J, Moule S, Murphy L, Oliver K, Osborne J, Quail MA, Rajandream MA, Rogers J, Rutter S, Seeger K, Skelton J, Squares R, Squares S, Sulston JE, Taylor K, Whitehead S, Barrell BG (- 32) Ref: Nature, 393:537, 1998 : PubMed ESTHER: Cole_1998_Nature_393_537 PubMedSearch: Cole 1998 Nature 393 537 PubMedID: 9634230 Gene_locus related to this paper: myctu-a85a, myctu-a85b, myctu-a85c, myctu-bpoC, myctu-cut3, myctu-cutas1, myctu-cutas2, myctu-d5yk66, myctu-ephA, myctu-ephB, myctu-ephc, myctu-ephd, myctu-ephE, myctu-ephF, myctu-hpx, myctu-linb, myctu-lipG, myctu-lipJ, myctu-LIPS, myctu-lipv, myctu-LPQC, myctu-LPQP, myctu-MBTB, myctu-metx, myctu-mpt51, myctu-MT1628, myctu-MT3441, myctu-p71654, myctu-p95011, myctu-PKS6, myctu-PKS13, myctu-ppe42, myctu-ppe63, myctu-Rv1430, myctu-RV0045C, myctu-Rv0077c, myctu-Rv0151c, myctu-Rv0152c, myctu-Rv0159c, myctu-Rv0160c, myctu-rv0183, myctu-Rv0217c, myctu-Rv0220, myctu-Rv0272c, myctu-RV0293C, myctu-RV0421C, myctu-RV0457C, myctu-RV0519C, myctu-RV0774C, myctu-RV0782, myctu-RV0840C, myctu-Rv1069c, myctu-Rv1076, myctu-RV1123C, myctu-Rv1184c, myctu-Rv1190, myctu-Rv1191, myctu-RV1192, myctu-RV1215C, myctu-Rv1399c, myctu-Rv1400c, myctu-Rv1426c, myctu-RV1639C, myctu-RV1683, myctu-RV1758, myctu-Rv1800, myctu-Rv1833c, myctu-RV2054, myctu-RV2296, myctu-Rv2385, myctu-Rv2485c, myctu-RV2627C, myctu-RV2672, myctu-RV2695, myctu-RV2765, myctu-RV2800, myctu-RV2854, myctu-Rv2970c, myctu-Rv3084, myctu-Rv3097c, myctu-rv3177, myctu-Rv3312c, myctu-RV3452, myctu-RV3473C, myctu-Rv3487c, myctu-Rv3569c, myctu-Rv3591c, myctu-RV3724, myctu-Rv3802c, myctu-Rv3822, myctu-y0571, myctu-y963, myctu-Y1834, myctu-y1835, myctu-y2079, myctu-Y2307, myctu-yc88, myctu-ym23, myctu-ym24, myctu-YR15, myctu-yt28 Abstract Countless millions of people have died from tuberculosis, a chronic infectious disease caused by the tubercle bacillus. The complete genome sequence of the best-characterized strain of Mycobacterium tuberculosis, H37Rv, has been determined and analysed in order to improve our understanding of the biology of this slow-growing pathogen and to help the conception of new prophylactic and therapeutic interventions. The genome comprises 4,411,529 base pairs, contains around 4,000 genes, and has a very high guanine + cytosine content that is reflected in the biased amino-acid content of the proteins. M. tuberculosis differs radically from other bacteria in that a very large portion of its coding capacity is devoted to the production of enzymes involved in lipogenesis and lipolysis, and to two new families of glycine-rich proteins with a repetitive structure that may represent a source of antigenic variation. Title: The nucleotide sequence of Saccharomyces cerevisiae chromosome XIII Bowman S, Churcher C, Badcock K, Brown D, Chillingworth T, Connor R, Dedman K, Devlin K, Gentles S and Barrell B <12 more author(s)> Bowman S, Churcher C, Badcock K, Brown D, Chillingworth T, Connor R, Dedman K, Devlin K, Gentles S, Hamlin N, Hunt S, Jagels K, Lye G, Moule S, Odell C, Pearson D, Rajandream M, Rice P, Skelton J, Walsh S, Whitehead S, Barrell B (- 12) Ref: Nature, 387:90, 1997 : PubMed ESTHER: Bowman_1997_Nature_387_90 PubMedSearch: Bowman 1997 Nature 387 90 PubMedID: 9169872 Gene_locus related to this paper: yeast-FSH2, yeast-ym60, yeast-ymc0 Abstract Systematic sequencing of the genome of Saccharomyces cerevisiae has revealed thousands of new predicted genes and allowed analysis of long-range features of chromosomal organization. Generally, genes and predicted genes seem to be distributed evenly throughout the genome, having no overall preference for DNA strand. Apart from the smaller chromosomes, which can have substantially lower gene density in their telomeric regions, there is a consistent average of one open reading frame (ORF) approximately every two kilobases. However, one of the most surprising findings for a eukaryote with approximately 6,000 genes was the amount of apparent redundancy in its genome. This redundancy occurs both between individual ORFs and over more extensive chromosome regions, which have been duplicated preserving gene order and orientation. Here we report the entire nucleotide sequence of chromosome XIII, the sixth-largest S. cerevisiae chromosome, and demonstrate that its features and organization are consistent with those observed for other S. cerevisiae chromosomes. Analysis revealed 459 ORFs, 284 have not been identified previously. Both intra- and interchromosomal duplications of regions of this chromosome have occurred. | |||||||
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