Author Report for: Simmonds MNo contact information in database for Simmonds M
Holden MT, Heather Z, Paillot R, Steward KF, Webb K, Ainslie F, Jourdan T, Bason NC, Holroyd NE and Waller AS <16 more author(s)> Holden MT, Heather Z, Paillot R, Steward KF, Webb K, Ainslie F, Jourdan T, Bason NC, Holroyd NE, Mungall K, Quail MA, Sanders M, Simmonds M, Willey D, Brooks K, Aanensen DM, Spratt BG, Jolley KA, Maiden MC, Kehoe M, Chanter N, Bentley SD, Robinson C, Maskell DJ, Parkhill J, Waller AS (- 16) Ref: PLoS Pathog, 5:e1000346, 2009 : PubMed ESTHER: Holden_2009_PLoS.Pathog_5_E1000346 PubMedSearch: Holden 2009 PLoS.Pathog 5 E1000346 PubMedID: 19325880 Gene_locus related to this paper: stre4-c0mbg3, stre4-pepx, strem-b4u0u4, strem-b4u3j8, strs7-pepx Abstract The continued evolution of bacterial pathogens has major implications for both human and animal disease, but the exchange of genetic material between host-restricted pathogens is rarely considered. Streptococcus equi subspecies equi (S. equi) is a host-restricted pathogen of horses that has evolved from the zoonotic pathogen Streptococcus equi subspecies zooepidemicus (S. zooepidemicus). These pathogens share approximately 80% genome sequence identity with the important human pathogen Streptococcus pyogenes. We sequenced and compared the genomes of S. equi 4047 and S. zooepidemicus H70 and screened S. equi and S. zooepidemicus strains from around the world to uncover evidence of the genetic events that have shaped the evolution of the S. equi genome and led to its emergence as a host-restricted pathogen. Our analysis provides evidence of functional loss due to mutation and deletion, coupled with pathogenic specialization through the acquisition of bacteriophage encoding a phospholipase A(2) toxin, and four superantigens, and an integrative conjugative element carrying a novel iron acquisition system with similarity to the high pathogenicity island of Yersinia pestis. We also highlight that S. equi, S. zooepidemicus, and S. pyogenes share a common phage pool that enhances cross-species pathogen evolution. We conclude that the complex interplay of functional loss, pathogenic specialization, and genetic exchange between S. equi, S. zooepidemicus, and S. pyogenes continues to influence the evolution of these important streptococci. Title: Pseudogene accumulation in the evolutionary histories of Salmonella enterica serovars Paratyphi A and Typhi Holt KE, Thomson NR, Wain J, Langridge GC, Hasan R, Bhutta ZA, Quail MA, Norbertczak H, Walker D and Parkhill J <5 more author(s)> Holt KE, Thomson NR, Wain J, Langridge GC, Hasan R, Bhutta ZA, Quail MA, Norbertczak H, Walker D, Simmonds M, White B, Bason N, Mungall K, Dougan G, Parkhill J (- 5) Ref: BMC Genomics, 10:36, 2009 : PubMed ESTHER: Holt_2009_BMC.Genomics_10_36 PubMedSearch: Holt 2009 BMC.Genomics 10 36 PubMedID: 19159446 Abstract BACKGROUND: Of the > 2000 serovars of Salmonella enterica subspecies I, most cause self-limiting gastrointestinal disease in a wide range of mammalian hosts. However, S. enterica serovars Typhi and Paratyphi A are restricted to the human host and cause the similar systemic diseases typhoid and paratyphoid fever. Genome sequence similarity between Paratyphi A and Typhi has been attributed to convergent evolution via relatively recent recombination of a quarter of their genomes. The accumulation of pseudogenes is a key feature of these and other host-adapted pathogens, and overlapping pseudogene complements are evident in Paratyphi A and Typhi. Title: Comparative genomics of the emerging human pathogen Photorhabdus asymbiotica with the insect pathogen Photorhabdus luminescens Wilkinson P, Waterfield NR, Crossman L, Corton C, Sanchez-Contreras M, Vlisidou I, Barron A, Bignell A, Clark L and ffrench-Constant RH <10 more author(s)> Wilkinson P, Waterfield NR, Crossman L, Corton C, Sanchez-Contreras M, Vlisidou I, Barron A, Bignell A, Clark L, Ormond D, Mayho M, Bason N, Smith F, Simmonds M, Churcher C, Harris D, Thompson NR, Quail M, Parkhill J, ffrench-Constant RH (- 10) Ref: BMC Genomics, 10:302, 2009 : PubMed ESTHER: Wilkinson_2009_BMC.Genomics_10_302 PubMedSearch: Wilkinson 2009 BMC.Genomics 10 302 PubMedID: 19583835 Gene_locus related to this paper: phoaa-b6vks1, phoaa-b6vmd3, phoaa-c7bgr2, phoaa-c7bhw5, phoaa-c7bjq6, phoaa-c7bk59, phoaa-c7bnd9, pholu-lxd2, pholu-PLU2437, phoaa-c7bh14, phoaa-c7bkb9 Abstract BACKGROUND: The Gram-negative bacterium Photorhabdus asymbiotica (Pa) has been recovered from human infections in both North America and Australia. Recently, Pa has been shown to have a nematode vector that can also infect insects, like its sister species the insect pathogen P. luminescens (Pl). To understand the relationship between pathogenicity to insects and humans in Photorhabdus we have sequenced the complete genome of Pa strain ATCC43949 from North America. This strain (formerly referred to as Xenorhabdus luminescens strain 2) was isolated in 1977 from the blood of an 80 year old female patient with endocarditis, in Maryland, USA. Here we compare the complete genome of Pa ATCC43949 with that of the previously sequenced insect pathogen P. luminescens strain TT01 which was isolated from its entomopathogenic nematode vector collected from soil in Trinidad and Tobago. RESULTS: We found that the human pathogen Pa had a smaller genome (5,064,808 bp) than that of the insect pathogen Pl (5,688,987 bp) but that each pathogen carries approximately one megabase of DNA that is unique to each strain. The reduced size of the Pa genome is associated with a smaller diversity in insecticidal genes such as those encoding the Toxin complexes (Tc's), Makes caterpillars floppy (Mcf) toxins and the Photorhabdus Virulence Cassettes (PVCs). The Pa genome, however, also shows the addition of a plasmid related to pMT1 from Yersinia pestis and several novel pathogenicity islands including a novel Type Three Secretion System (TTSS) encoding island. Together these data suggest that Pa may show virulence against man via the acquisition of the pMT1-like plasmid and specific effectors, such as SopB, that promote its persistence inside human macrophages. Interestingly the loss of insecticidal genes in Pa is not reflected by a loss of pathogenicity towards insects. CONCLUSION: Our results suggest that North American isolates of Pa have acquired virulence against man via the acquisition of a plasmid and specific virulence factors with similarity to those shown to play roles in pathogenicity against humans in other bacteria. Title: The genome of the simian and human malaria parasite Plasmodium knowlesi 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: 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 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 social amoeba Dictyostelium discoideum Eichinger L, Pachebat JA, Glockner G, Rajandream MA, Sucgang R, Berriman M, Song J, Olsen R, Szafranski K and Kuspa A <87 more author(s)> Eichinger L, Pachebat JA, Glockner G, Rajandream MA, Sucgang R, Berriman M, Song J, Olsen R, Szafranski K, Xu Q, Tunggal B, Kummerfeld S, Madera M, Konfortov BA, Rivero F, Bankier AT, Lehmann R, Hamlin N, Davies R, Gaudet P, Fey P, Pilcher K, Chen G, Saunders D, Sodergren E, Davis P, Kerhornou A, Nie X, Hall N, Anjard C, Hemphill L, Bason N, Farbrother P, Desany B, Just E, Morio T, Rost R, Churcher C, Cooper J, Haydock S, van Driessche N, Cronin A, Goodhead I, Muzny D, Mourier T, Pain A, Lu M, Harper D, Lindsay R, Hauser H, James K, Quiles M, Madan Babu M, Saito T, Buchrieser C, Wardroper A, Felder M, Thangavelu M, Johnson D, Knights A, Loulseged H, Mungall K, Oliver K, Price C, Quail MA, Urushihara H, Hernandez J, Rabbinowitsch E, Steffen D, Sanders M, Ma J, Kohara Y, Sharp S, Simmonds M, Spiegler S, Tivey A, Sugano S, White B, Walker D, Woodward J, Winckler T, Tanaka Y, Shaulsky G, Schleicher M, Weinstock G, Rosenthal A, Cox EC, Chisholm RL, Gibbs R, Loomis WF, Platzer M, Kay RR, Williams J, Dear PH, Noegel AA, Barrell B, Kuspa A (- 87) Ref: Nature, 435:43, 2005 : PubMed ESTHER: Eichinger_2005_Nature_435_43 PubMedSearch: Eichinger 2005 Nature 435 43 PubMedID: 15875012 Gene_locus related to this paper: dicdi-abhd, dicdi-ACHE, dicdi-apra, dicdi-cinbp, dicdi-CMBL, dicdi-crysp, dicdi-DPOA, dicdi-P90528, dicdi-ppme1, dicdi-Q8MYE7, dicdi-q54cf7, dicdi-q54cl7, dicdi-q54cm0, dicdi-q54ct5, dicdi-q54cu1, dicdi-q54d54, dicdi-q54d66, dicdi-q54dj5, dicdi-q54dy7, dicdi-q54ek1, dicdi-q54eq6, dicdi-q54et1, dicdi-q54et7, dicdi-q54f01, dicdi-q54g24, dicdi-q54g47, dicdi-q54gi7, dicdi-q54gw5, dicdi-q54gx3, dicdi-q54h23, dicdi-q54h73, dicdi-q54i38, dicdi-q54ie5, dicdi-q54in4, dicdi-q54kz1, dicdi-q54l36, dicdi-q54li1, dicdi-q54m29, dicdi-q54n21, dicdi-q54n35, dicdi-q54n85, dicdi-q54qe7, dicdi-q54qi3, dicdi-q54qk2, dicdi-q54rl3, dicdi-q54rl8, dicdi-q54sy6, dicdi-q54sz3, dicdi-q54t49, dicdi-q54t91, dicdi-q54th2, dicdi-q54u01, dicdi-q54vc2, dicdi-q54vw1, dicdi-q54xe3, dicdi-q54xl3, dicdi-q54xu1, dicdi-q54xu2, dicdi-q54y48, dicdi-q54yd0, dicdi-q54ye0, dicdi-q54yl1, dicdi-q54yr8, dicdi-q54z90, dicdi-q55bx3, dicdi-q55d01, dicdi-q55d81, dicdi-q55du6, dicdi-q55eu1, dicdi-q55eu8, dicdi-q55fk4, dicdi-q55gk7, dicdi-Q54ZA6, dicdi-q86h82, dicdi-Q86HC9, dicdi-Q86HM5, dicdi-Q86HM6, dicdi-q86iz7, dicdi-q86jb6, dicdi-Q86KU7, dicdi-q550s3, dicdi-q552c0, dicdi-q553t5, dicdi-q555e5, dicdi-q555h0, dicdi-q555h1, dicdi-q557k5, dicdi-q558u2, dicdi-Q869Q8, dicdi-u554, dicdi-y9086, dicdi-q54r44, dicdi-f172a Abstract The social amoebae are exceptional in their ability to alternate between unicellular and multicellular forms. Here we describe the genome of the best-studied member of this group, Dictyostelium discoideum. The gene-dense chromosomes of this organism encode approximately 12,500 predicted proteins, a high proportion of which have long, repetitive amino acid tracts. There are many genes for polyketide synthases and ABC transporters, suggesting an extensive secondary metabolism for producing and exporting small molecules. The genome is rich in complex repeats, one class of which is clustered and may serve as centromeres. Partial copies of the extrachromosomal ribosomal DNA (rDNA) element are found at the ends of each chromosome, suggesting a novel telomere structure and the use of a common mechanism to maintain both the rDNA and chromosomal termini. A proteome-based phylogeny shows that the amoebozoa diverged from the animal-fungal lineage after the plant-animal split, but Dictyostelium seems to have retained more of the diversity of the ancestral genome than have plants, animals or fungi. 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: 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. | |||||||
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