Author Report for: Harris DNo contact information in database for Harris D
Uslaner JM, Kuduk SD, Wittmann M, Lange HS, Fox SV, Min C, Pajkovic N, Harris D, Cilissen C and Beshore DC <3 more author(s)> Uslaner JM, Kuduk SD, Wittmann M, Lange HS, Fox SV, Min C, Pajkovic N, Harris D, Cilissen C, Mahon C, Mostoller K, Warrington S, Beshore DC (- 3) Ref: Journal of Pharmacology & Experimental Therapeutics, 365:556, 2018 : PubMed ESTHER: Uslaner_2018_J.Pharmacol.Exp.Ther_365_556 PubMedSearch: Uslaner 2018 J.Pharmacol.Exp.Ther 365 556 PubMedID: 29563325 Abstract The current standard of care for treating Alzheimer's disease is acetylcholinesterase inhibitors, which nonselectively increase cholinergic signaling by indirectly enhancing activity of nicotinic and muscarinic receptors. These drugs improve cognitive function in patients, but also produce unwanted side effects that limit their efficacy. In an effort to selectively improve cognition and avoid the cholinergic side effects associated with the standard of care, various efforts have been aimed at developing selective M1 muscarinic receptor activators. In this work, we describe the preclinical and clinical pharmacodynamic effects of the M1 muscarinic receptor-positive allosteric modulator, MK-7622. MK-7622 attenuated the cognitive-impairing effects of the muscarinic receptor antagonist scopolamine and altered quantitative electroencephalography (qEEG) in both rhesus macaque and human. For both scopolamine reversal and qEEG, the effective exposures were similar between species. However, across species the minimum effective exposures to attenuate the scopolamine impairment were lower than for qEEG. Additionally, there were differences in the spectral power changes produced by MK-7622 in rhesus versus human. In sum, these results are the first to demonstrate translation of preclinical cognition and target modulation to clinical effects in humans for a selective M1 muscarinic receptor-positive allosteric modulator. Title: Comparative genomics of the apicomplexan parasites Toxoplasma gondii and Neospora caninum: Coccidia differing in host range and transmission strategy Reid AJ, Vermont SJ, Cotton JA, Harris D, Hill-Cawthorne GA, Konen-Waisman S, Latham SM, Mourier T, Norton R and Wastling JM <13 more author(s)> Reid AJ, Vermont SJ, Cotton JA, Harris D, Hill-Cawthorne GA, Konen-Waisman S, Latham SM, Mourier T, Norton R, Quail MA, Sanders M, Shanmugam D, Sohal A, Wasmuth JD, Brunk B, Grigg ME, Howard JC, Parkinson J, Roos DS, Trees AJ, Berriman M, Pain A, Wastling JM (- 13) Ref: PLoS Pathog, 8:e1002567, 2012 : PubMed ESTHER: Reid_2012_PLoS.Pathog_8_e1002567 PubMedSearch: Reid 2012 PLoS.Pathog 8 e1002567 PubMedID: 22457617 Gene_locus related to this paper: neocl-f0v9d7, neocl-f0v729, neocl-f0vc02, neocl-f0vce2, neocl-f0vq55 Abstract Toxoplasma gondii is a zoonotic protozoan parasite which infects nearly one third of the human population and is found in an extraordinary range of vertebrate hosts. Its epidemiology depends heavily on horizontal transmission, especially between rodents and its definitive host, the cat. Neospora caninum is a recently discovered close relative of Toxoplasma, whose definitive host is the dog. Both species are tissue-dwelling Coccidia and members of the phylum Apicomplexa; they share many common features, but Neospora neither infects humans nor shares the same wide host range as Toxoplasma, rather it shows a striking preference for highly efficient vertical transmission in cattle. These species therefore provide a remarkable opportunity to investigate mechanisms of host restriction, transmission strategies, virulence and zoonotic potential. We sequenced the genome of N. caninum and transcriptomes of the invasive stage of both species, undertaking an extensive comparative genomics and transcriptomics analysis. We estimate that these organisms diverged from their common ancestor around 28 million years ago and find that both genomes and gene expression are remarkably conserved. However, in N. caninum we identified an unexpected expansion of surface antigen gene families and the divergence of secreted virulence factors, including rhoptry kinases. Specifically we show that the rhoptry kinase ROP18 is pseudogenised in N. caninum and that, as a possible consequence, Neospora is unable to phosphorylate host immunity-related GTPases, as Toxoplasma does. This defense strategy is thought to be key to virulence in Toxoplasma. We conclude that the ecological niches occupied by these species are influenced by a relatively small number of gene products which operate at the host-parasite interface and that the dominance of vertical transmission in N. caninum may be associated with the evolution of reduced virulence in this species. Title: Chromosome and gene copy number variation allow major structural change between species and strains of Leishmania Rogers MB, Hilley JD, Dickens NJ, Wilkes J, Bates PA, Depledge DP, Harris D, Her Y, Herzyk P and Mottram JC <8 more author(s)> Rogers MB, Hilley JD, Dickens NJ, Wilkes J, Bates PA, Depledge DP, Harris D, Her Y, Herzyk P, Imamura H, Otto TD, Sanders M, Seeger K, Dujardin JC, Berriman M, Smith DF, Hertz-Fowler C, Mottram JC (- 8) Ref: Genome Res, 21:2129, 2011 : PubMed ESTHER: Rogers_2011_Genome.Res_21_2129 PubMedSearch: Rogers 2011 Genome.Res 21 2129 PubMedID: 22038252 Abstract Leishmania parasites cause a spectrum of clinical pathology in humans ranging from disfiguring cutaneous lesions to fatal visceral leishmaniasis. We have generated a reference genome for Leishmania mexicana and refined the reference genomes for Leishmania major, Leishmania infantum, and Leishmania braziliensis. This has allowed the identification of a remarkably low number of genes or paralog groups (2, 14, 19, and 67, respectively) unique to one species. These were found to be conserved in additional isolates of the same species. We have predicted allelic variation and find that in these isolates, L. major and L. infantum have a surprisingly low number of predicted heterozygous SNPs compared with L. braziliensis and L. mexicana. We used short read coverage to infer ploidy and gene copy numbers, identifying large copy number variations between species, with 200 tandem gene arrays in L. major and 132 in L. mexicana. Chromosome copy number also varied significantly between species, with nine supernumerary chromosomes in L. infantum, four in L. mexicana, two in L. braziliensis, and one in L. major. A significant bias against gene arrays on supernumerary chromosomes was shown to exist, indicating that duplication events occur more frequently on disomic chromosomes. Taken together, our data demonstrate that there is little variation in unique gene content across Leishmania species, but large-scale genetic heterogeneity can result through gene amplification on disomic chromosomes and variation in chromosome number. Increased gene copy number due to chromosome amplification may contribute to alterations in gene expression in response to environmental conditions in the host, providing a genetic basis for disease tropism. Title: Evolution of pathogenicity and sexual reproduction in eight Candida genomes Butler G, Rasmussen MD, Lin MF, Santos MA, Sakthikumar S, Munro CA, Rheinbay E, Grabherr M, Forche A and Cuomo CA <41 more author(s)> Butler G, Rasmussen MD, Lin MF, Santos MA, Sakthikumar S, Munro CA, Rheinbay E, Grabherr M, Forche A, Reedy JL, Agrafioti I, Arnaud MB, Bates S, Brown AJ, Brunke S, Costanzo MC, Fitzpatrick DA, de Groot PW, Harris D, Hoyer LL, Hube B, Klis FM, Kodira C, Lennard N, Logue ME, Martin R, Neiman AM, Nikolaou E, Quail MA, Quinn J, Santos MC, Schmitzberger FF, Sherlock G, Shah P, Silverstein KA, Skrzypek MS, Soll D, Staggs R, Stansfield I, Stumpf MP, Sudbery PE, Srikantha T, Zeng Q, Berman J, Berriman M, Heitman J, Gow NA, Lorenz MC, Birren BW, Kellis M, Cuomo CA (- 41) Ref: Nature, 459:657, 2009 : PubMed ESTHER: Butler_2009_Nature_459_657 PubMedSearch: Butler 2009 Nature 459 657 PubMedID: 19465905 Gene_locus related to this paper: canal-ATG15, canal-bna7, canal-c4yl13, canal-LIP1, canal-LIP2, canal-LIP3, canal-LIP4, canal-LIP5, canal-LIP6, canal-LIP7, canal-LIP8, canal-LIP9, canal-LIP10, canal-ppme1, canal-q5a0c9, canal-q5a2i9, canal-q5a042, canal-q5ad17, canal-q5aeu3, canal-q5afp8, canal-q5ag57, canal-q5ai09, canal-q5ai12, canal-q5ajt3, canal-q5akz5, canal-q5apu4, canal-q59l46, canal-q59m48, canal-q59nw6, canal-q59u61, canal-q59u64, canal-q59vp0, canal-q59y97, canaw-c4ykb1, canaw-c4yrn6, canaw-c4yrn9, canaw-c4yrr3, canaw-c4yrv3, canaw-c4ys26, cantt-c5m3d7, cantt-c5m3y5, cantt-c5m4x0, cantt-c5m5e8, cantt-c5m5w2, cantt-c5m8s7, cantt-c5m9c2, cantt-c5m465, cantt-c5m751, cantt-c5m793, cantt-c5m893, cantt-c5ma78, cantt-c5mag0, cantt-c5mbb8, cantt-c5mc53, cantt-c5md87, cantt-c5mdy3, cantt-c5mey7, cantt-c5mfg0, cantt-c5mfh8, cantt-c5mg56, cantt-c5mgj0, cantt-c5mh75, cantt-c5mh80, cantt-c5mh89, cantt-c5mhh0, cantt-c5mhn5, cantt-c5mij5, cantt-c5min7, clal4-c4xvt8, clal4-c4xwy4, clal4-c4xy03, clal4-c4xyx9, clal4-c4xzz1, clal4-c4y3e1, clal4-c4y4f2, clal4-c4y4w8, clal4-c4y5j4, clal4-c4y5j9, clal4-c4y7z7, clal4-c4y8q1, clal4-c4y035, clal4-c4y481, clal4-c4y538, clal4-c4y898, clal4-c4yas2, clal4-c4yba6, clal4-c4yba7, clal4-c4yc85, lodel-a5drz3, lodel-a5ds97, lodel-a5dsc0, lodel-a5duu4, lodel-a5duy7, lodel-a5dv03, lodel-a5dv46, lodel-a5dw16, lodel-a5dwv7, lodel-a5dww6, lodel-a5dxf3, lodel-a5e0z5, lodel-a5e1c1, lodel-a5e1l4, lodel-a5e1p3, lodel-a5e2s1, lodel-a5e2t8, lodel-a5e2v2, lodel-a5e4u8, lodel-a5e5a9, lodel-a5e5k1, lodel-a5e5z7, lodel-a5e6w1, lodel-a5e028, lodel-atg15, lodel-kex1, picgu-a5d9u2, picgu-a5dav0, picgu-a5dbk0, picgu-a5dc45, picgu-a5dc73, picgu-a5dc74, picgu-a5dc75, picgu-a5ddt8, picgu-a5dev7, picgu-a5dh90, picgu-a5dhe3, picgu-a5di38, picgu-a5dj06, picgu-a5dkd8, picgu-a5dle9, picgu-a5dlj5, picgu-a5dm19, picgu-a5dn92, picgu-a5dnr3, picgu-a5dnt6, picgu-a5dqu5, picgu-a5dr14, picgu-a5drl3, picgu-atg15, picgu-bna7, picgu-a5d9q3, picgu-a5dag9, clal4-c4y5a2, clal4-c4y0l0, cantt-c5mcb1, clal4-c4y8j2, cantt-c5m494, clals-a0a202gac7, canal-hda1, picgu-a5dks8, lodel-a5drs6, canpc-g8bbk1, cantt-kex1, clal4-kex1, picgu-kex1 Abstract Candida species are the most common cause of opportunistic fungal infection worldwide. Here we report the genome sequences of six Candida species and compare these and related pathogens and non-pathogens. There are significant expansions of cell wall, secreted and transporter gene families in pathogenic species, suggesting adaptations associated with virulence. Large genomic tracts are homozygous in three diploid species, possibly resulting from recent recombination events. Surprisingly, key components of the mating and meiosis pathways are missing from several species. These include major differences at the mating-type loci (MTL); Lodderomyces elongisporus lacks MTL, and components of the a1/2 cell identity determinant were lost in other species, raising questions about how mating and cell types are controlled. Analysis of the CUG leucine-to-serine genetic-code change reveals that 99% of ancestral CUG codons were erased and new ones arose elsewhere. Lastly, we revise the Candida albicans gene catalogue, identifying many new genes. Title: Complete genome sequence and comparative genome analysis of enteropathogenic Escherichia coli O127:H6 strain E2348/69 Iguchi A, Thomson NR, Ogura Y, Saunders D, Ooka T, Henderson IR, Harris D, Asadulghani M, Kurokawa K and Frankel G <7 more author(s)> Iguchi A, Thomson NR, Ogura Y, Saunders D, Ooka T, Henderson IR, Harris D, Asadulghani M, Kurokawa K, Dean P, Kenny B, Quail MA, Thurston S, Dougan G, Hayashi T, Parkhill J, Frankel G (- 7) Ref: Journal of Bacteriology, 191:347, 2009 : PubMed ESTHER: Iguchi_2009_J.Bacteriol_191_347 PubMedSearch: Iguchi 2009 J.Bacteriol 191 347 PubMedID: 18952797 Gene_locus related to this paper: ecoli-Aes, ecoli-rutD, ecoli-bioh, ecoli-C0410, ecoli-C4836, ecoli-dlhh, ecoli-entf, ecoli-fes, ecoli-pldb, ecoli-ptrb, ecoli-yafa, ecoli-yaim, ecoli-ybff, ecoli-ycfp, ecoli-ycjy, ecoli-yeiG, ecoli-YFBB, ecoli-yghX, ecoli-yhet, ecoli-yiel, ecoli-yjfp, ecoli-ypfh, ecoli-ypt1, ecoli-yqia, ecoli-YfhR Abstract Enteropathogenic Escherichia coli (EPEC) was the first pathovar of E. coli to be implicated in human disease; however, no EPEC strain has been fully sequenced until now. Strain E2348/69 (serotype O127:H6 belonging to E. coli phylogroup B2) has been used worldwide as a prototype strain to study EPEC biology, genetics, and virulence. Studies of E2348/69 led to the discovery of the locus of enterocyte effacement-encoded type III secretion system (T3SS) and its cognate effectors, which play a vital role in attaching and effacing lesion formation on gut epithelial cells. In this study, we determined the complete genomic sequence of E2348/69 and performed genomic comparisons with other important E. coli strains. We identified 424 E2348/69-specific genes, most of which are carried on mobile genetic elements, and a number of genetic traits specifically conserved in phylogroup B2 strains irrespective of their pathotypes, including the absence of the ETT2-related T3SS, which is present in E. coli strains belonging to all other phylogroups. The genome analysis revealed the entire gene repertoire related to E2348/69 virulence. Interestingly, E2348/69 contains only 21 intact T3SS effector genes, all of which are carried on prophages and integrative elements, compared to over 50 effector genes in enterohemorrhagic E. coli O157. As E2348/69 is the most-studied pathogenic E. coli strain, this study provides a genomic context for the vast amount of existing experimental data. The unexpected simplicity of the E2348/69 T3SS provides the first opportunity to fully dissect the entire virulence strategy of attaching and effacing pathogens in the genomic context. Title: Comparative genomics of the fungal pathogens Candida dubliniensis and Candida albicans Jackson AP, Gamble JA, Yeomans T, Moran GP, Saunders D, Harris D, Aslett M, Barrell JF, Butler G and Berriman M <16 more author(s)> Jackson AP, Gamble JA, Yeomans T, Moran GP, Saunders D, Harris D, Aslett M, Barrell JF, Butler G, Citiulo F, Coleman DC, de Groot PW, Goodwin TJ, Quail MA, McQuillan J, Munro CA, Pain A, Poulter RT, Rajandream MA, Renauld H, Spiering MJ, Tivey A, Gow NA, Barrell B, Sullivan DJ, Berriman M (- 16) Ref: Genome Res, 19:2231, 2009 : PubMed ESTHER: Jackson_2009_Genome.Res_19_2231 PubMedSearch: Jackson 2009 Genome.Res 19 2231 PubMedID: 19745113 Gene_locus related to this paper: canal-ATG15, canal-c4yl13, canal-ppme1, canal-q5a0c9, canal-q5ad17, canal-q5ady2, canal-q5ag57, canal-q5ai12, canal-q5akz5, canal-q5apu4, canal-q59m48, canal-q59nw6, candc-b9w8x6, candc-b9w8x7, candc-b9w905, candc-b9wa64, candc-b9wc27, candc-b9wc30, candc-b9wc93, candc-b9wce3, candc-b9wdh9, candc-b9wds3, candc-b9whs3, candc-b9whs6, candc-b9whv2, candc-b9wi60, candc-b9wid3, candc-b9wje5, candc-b9wk97, candc-CduLAc, candc-b9wkf5, candc-b9wkj1, candc-b9wlf0, candc-b9wmt8, candc-b9wmx4, candc-b9wc51, candc-b9wa43, candc-b9wl19, candc-kex1 Abstract Candida dubliniensis is the closest known relative of Candida albicans, the most pathogenic yeast species in humans. However, despite both species sharing many phenotypic characteristics, including the ability to form true hyphae, C. dubliniensis is a significantly less virulent and less versatile pathogen. Therefore, to identify C. albicans-specific genes that may be responsible for an increased capacity to cause disease, we have sequenced the C. dubliniensis genome and compared it with the known C. albicans genome sequence. Although the two genome sequences are highly similar and synteny is conserved throughout, 168 species-specific genes are identified, including some encoding known hyphal-specific virulence factors, such as the aspartyl proteinases Sap4 and Sap5 and the proposed invasin Als3. Among the 115 pseudogenes confirmed in C. dubliniensis are orthologs of several filamentous growth regulator (FGR) genes that also have suspected roles in pathogenesis. However, the principal differences in genomic repertoire concern expansion of the TLO gene family of putative transcription factors and the IFA family of putative transmembrane proteins in C. albicans, which represent novel candidate virulence-associated factors. The results suggest that the recent evolutionary histories of C. albicans and C. dubliniensis are quite different. While gene families instrumental in pathogenesis have been elaborated in C. albicans, C. dubliniensis has lost genomic capacity and key pathogenic functions. This could explain why C. albicans is a more potent pathogen in humans than C. dubliniensis. Title: Epidemic multiple drug resistant Salmonella Typhimurium causing invasive disease in sub-Saharan Africa have a distinct genotype Kingsley RA, Msefula CL, Thomson NR, Kariuki S, Holt KE, Gordon MA, Harris D, Clarke L, Whitehead S and Dougan G <8 more author(s)> Kingsley RA, Msefula CL, Thomson NR, Kariuki S, Holt KE, Gordon MA, Harris D, Clarke L, Whitehead S, Sangal V, Marsh K, Achtman M, Molyneux ME, Cormican M, Parkhill J, MacLennan CA, Heyderman RS, Dougan G (- 8) Ref: Genome Res, 19:2279, 2009 : PubMed ESTHER: Kingsley_2009_Genome.Res_19_2279 PubMedSearch: Kingsley 2009 Genome.Res 19 2279 PubMedID: 19901036 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 Whereas most nontyphoidal Salmonella (NTS) are associated with gastroenteritis, there has been a dramatic increase in reports of NTS-associated invasive disease in sub-Saharan Africa. Salmonella enterica serovar Typhimurium isolates are responsible for a significant proportion of the reported invasive NTS in this region. Multilocus sequence analysis of invasive S. Typhimurium from Malawi and Kenya identified a dominant type, designated ST313, which currently is rarely reported outside of Africa. Whole-genome sequencing of a multiple drug resistant (MDR) ST313 NTS isolate, D23580, identified a distinct prophage repertoire and a composite genetic element encoding MDR genes located on a virulence-associated plasmid. Further, there was evidence of genome degradation, including pseudogene formation and chromosomal deletions, when compared with other S. Typhimurium genome sequences. Some of this genome degradation involved genes previously implicated in virulence of S. Typhimurium or genes for which the orthologs in S. Typhi are either pseudogenes or are absent. Genome analysis of other epidemic ST313 isolates from Malawi and Kenya provided evidence for microevolution and clonal replacement in the field. Title: Genomic and genetic analyses of diversity and plant interactions of Pseudomonas fluorescens Silby MW, Cerdeno-Tarraga AM, Vernikos GS, Giddens SR, Jackson RW, Preston GM, Zhang XX, Moon CD, Gehrig SM and Thomson NR <24 more author(s)> Silby MW, Cerdeno-Tarraga AM, Vernikos GS, Giddens SR, Jackson RW, Preston GM, Zhang XX, Moon CD, Gehrig SM, Godfrey SA, Knight CG, Malone JG, Robinson Z, Spiers AJ, Harris S, Challis GL, Yaxley AM, Harris D, Seeger K, Murphy L, Rutter S, Squares R, Quail MA, Saunders E, Mavromatis K, Brettin TS, Bentley SD, Hothersall J, Stephens E, Thomas CM, Parkhill J, Levy SB, Rainey PB, Thomson NR (- 24) Ref: Genome Biol, 10:R51, 2009 : PubMed ESTHER: Silby_2009_Genome.Biol_10_R51 PubMedSearch: Silby 2009 Genome.Biol 10 R51 PubMedID: 19432983 Gene_locus related to this paper: psef5-metx, psefl-este, psefs-c3jz63, psefs-c3jzq8, psefs-c3k1v7, psefs-c3k3d6, psefs-c3k3m8, psefs-c3k3s9, psefs-c3k5q5, psefs-c3k6c6, psefs-c3k7v4, psefs-c3k8m7, psefs-c3k8y7, psefs-c3k9z2, psefs-c3k032, psefs-c3k320, psefs-c3k362, psefs-c3k632, psefs-c3k927, psefs-c3kan9, psefs-c3kbe5, psefs-c3kdh9, psefs-c3ke34, psefs-laaa, psepf-q3k5t9, psepf-q3k6f3, psepf-q3k524, psepf-q3kcu9, psepf-q3kd07, psepf-q3kf33, psepf-q3kh87, psefs-c3jxp6, psepf-q3kf85, psefs-c3k813, psefs-c3keb8, psefl-e2xkc8, psefs-c3k9x6 Abstract BACKGROUND: Pseudomonas fluorescens are common soil bacteria that can improve plant health through nutrient cycling, pathogen antagonism and induction of plant defenses. The genome sequences of strains SBW25 and Pf0-1 were determined and compared to each other and with P. fluorescens Pf-5. A functional genomic in vivo expression technology (IVET) screen provided insight into genes used by P. fluorescens in its natural environment and an improved understanding of the ecological significance of diversity within this species. RESULTS: Comparisons of three P. fluorescens genomes (SBW25, Pf0-1, Pf-5) revealed considerable divergence: 61% of genes are shared, the majority located near the replication origin. Phylogenetic and average amino acid identity analyses showed a low overall relationship. A functional screen of SBW25 defined 125 plant-induced genes including a range of functions specific to the plant environment. Orthologues of 83 of these exist in Pf0-1 and Pf-5, with 73 shared by both strains. The P. fluorescens genomes carry numerous complex repetitive DNA sequences, some resembling Miniature Inverted-repeat Transposable Elements (MITEs). In SBW25, repeat density and distribution revealed 'repeat deserts' lacking repeats, covering approximately 40% of the genome. CONCLUSIONS: P. fluorescens genomes are highly diverse. Strain-specific regions around the replication terminus suggest genome compartmentalization. The genomic heterogeneity among the three strains is reminiscent of a species complex rather than a single species. That 42% of plant-inducible genes were not shared by all strains reinforces this conclusion and shows that ecological success requires specialized and core functions. The diversity also indicates the significant size of genetic information within the Pseudomonas pan genome. 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: Newly introduced genomic prophage islands are critical determinants of in vivo competitiveness in the Liverpool Epidemic Strain of Pseudomonas aeruginosa Winstanley C, Langille MG, Fothergill JL, Kukavica-Ibrulj I, Paradis-Bleau C, Sanschagrin F, Thomson NR, Winsor GL, Quail MA and Levesque RC <9 more author(s)> Winstanley C, Langille MG, Fothergill JL, Kukavica-Ibrulj I, Paradis-Bleau C, Sanschagrin F, Thomson NR, Winsor GL, Quail MA, Lennard N, Bignell A, Clarke L, Seeger K, Saunders D, Harris D, Parkhill J, Hancock RE, Brinkman FS, Levesque RC (- 9) Ref: Genome Res, 19:12, 2009 : PubMed ESTHER: Winstanley_2009_Genome.Res_19_12 PubMedSearch: Winstanley 2009 Genome.Res 19 12 PubMedID: 19047519 Gene_locus related to this paper: pseae-clipa, pseae-CPO, pseae-llipa, pseae-metx, pseae-PA0201, pseae-PA0231, pseae-PA0308, pseae-PA0368, pseae-PA0480, pseae-PA0502, pseae-PA0543, pseae-PA0599, pseae-PA1166, pseae-PA1291, pseae-PA1304, pseae-PA1510, pseae-PA1558, pseae-PA1597, pseae-PA1907, pseae-PA2086, pseae-PA2098, pseae-PA2302, pseae-PA2425, pseae-PA2451, pseae-PA2540, pseae-PA2682, pseae-PA2689, pseae-PA2745, pseae-PA2764, pseae-PA2927, pseae-PA2934, pseae-PA2949, pseae-PA3132, pseae-PA3301, pseae-PA3324, pseae-PA3327, pseae-PA3429, pseae-PA3586, pseae-PA3628, pseae-PA3695, pseae-PA3859, pseae-PA3994, pseae-PA4152, pseae-PA4968, pseae-PA5080, pseae-PCHC, pseae-PCHF, pseae-PHAC2, pseae-phaD, pseae-phag, pseae-Q9APW4, pseae-rhla, pseae-q9i252 Abstract Pseudomonas aeruginosa isolates have a highly conserved core genome representing up to 90% of the total genomic sequence with additional variable accessory genes, many of which are found in genomic islands or islets. The identification of the Liverpool Epidemic Strain (LES) in a children's cystic fibrosis (CF) unit in 1996 and its subsequent observation in several centers in the United Kingdom challenged the previous widespread assumption that CF patients acquire only unique strains of P. aeruginosa from the environment. To learn about the forces that shaped the development of this important epidemic strain, the genome of the earliest archived LES isolate, LESB58, was sequenced. The sequence revealed the presence of many large genomic islands, including five prophage clusters, one defective (pyocin) prophage cluster, and five non-phage islands. To determine the role of these clusters, an unbiased signature tagged mutagenesis study was performed, followed by selection in the chronic rat lung infection model. Forty-seven mutants were identified by sequencing, including mutants in several genes known to be involved in Pseudomonas infection. Furthermore, genes from four prophage clusters and one genomic island were identified and in direct competition studies with the parent isolate; four were demonstrated to strongly impact on competitiveness in the chronic rat lung infection model. This strongly indicates that enhanced in vivo competitiveness is a major driver for maintenance and diversifying selection of these genomic prophage genes. Title: The complete genome, comparative and functional analysis of Stenotrophomonas maltophilia reveals an organism heavily shielded by drug resistance determinants Crossman LC, Gould VC, Dow JM, Vernikos GS, Okazaki A, Sebaihia M, Saunders D, Arrowsmith C, Carver T and Avison MB <15 more author(s)> Crossman LC, Gould VC, Dow JM, Vernikos GS, Okazaki A, Sebaihia M, Saunders D, Arrowsmith C, Carver T, Peters N, Adlem E, Kerhornou A, Lord A, Murphy L, Seeger K, Squares R, Rutter S, Quail MA, Rajandream MA, Harris D, Churcher C, Bentley SD, Parkhill J, Thomson NR, Avison MB (- 15) Ref: Genome Biol, 9:R74, 2008 : PubMed ESTHER: Crossman_2008_Genome.Biol_9_R74 PubMedSearch: Crossman 2008 Genome.Biol 9 R74 PubMedID: 18419807 Gene_locus related to this paper: strm5-b4sjf3, strm5-b4sly1, strm5-b4smq6, strm5-b4st20, strm5-bioh, strmk-b2fhb1, strmk-b2fju9, strmk-b2fkx8, strmk-b2fl50, strmk-b2fl54, strmk-b2flj0, strmk-b2fnc5, strmk-b2fre3, strmk-b2frm1, strmk-b2frs0, strmk-b2fsp0, strmk-b2ftw9, strmk-b2fuf3, strmk-metx, xanma-P95782, strmk-b2fmj5, strmk-b2fpy9, strmk-b2ftk7, strmk-b2frv5 Abstract BACKGROUND: Stenotrophomonas maltophilia is a nosocomial opportunistic pathogen of the Xanthomonadaceae. The organism has been isolated from both clinical and soil environments in addition to the sputum of cystic fibrosis patients and the immunocompromised. Whilst relatively distant phylogenetically, the closest sequenced relatives of S. maltophilia are the plant pathogenic xanthomonads. RESULTS: The genome of the bacteremia-associated isolate S. maltophilia K279a is 4,851,126 bp and of high G+C content. The sequence reveals an organism with a remarkable capacity for drug and heavy metal resistance. In addition to a number of genes conferring resistance to antimicrobial drugs of different classes via alternative mechanisms, nine resistance-nodulation-division (RND)-type putative antimicrobial efflux systems are present. Functional genomic analysis confirms a role in drug resistance for several of the novel RND efflux pumps. S. maltophilia possesses potentially mobile regions of DNA and encodes a number of pili and fimbriae likely to be involved in adhesion and biofilm formation that may also contribute to increased antimicrobial drug resistance. CONCLUSION: The panoply of antimicrobial drug resistance genes and mobile genetic elements found suggests that the organism can act as a reservoir of antimicrobial drug resistance determinants in a clinical environment, which is an issue of considerable concern. Title: The genome sequence of the fish pathogen Aliivibrio salmonicida strain LFI1238 shows extensive evidence of gene decay Hjerde E, Lorentzen MS, Holden MT, Seeger K, Paulsen S, Bason N, Churcher C, Harris D, Norbertczak H and Thomson NR <5 more author(s)> Hjerde E, Lorentzen MS, Holden MT, Seeger K, Paulsen S, Bason N, Churcher C, Harris D, Norbertczak H, Quail MA, Sanders S, Thurston S, Parkhill J, Willassen NP, Thomson NR (- 5) Ref: BMC Genomics, 9:616, 2008 : PubMed ESTHER: Hjerde_2008_BMC.Genomics_9_616 PubMedSearch: Hjerde 2008 BMC.Genomics 9 616 PubMedID: 19099551 Gene_locus related to this paper: alisl-b6elz2, alisl-b6ek45 Abstract BACKGROUND: The fish pathogen Aliivibrio salmonicida is the causative agent of cold-water vibriosis in marine aquaculture. The Gram-negative bacterium causes tissue degradation, hemolysis and sepsis in vivo. 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: 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: 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: Comparison of the genome sequence of the poultry pathogen Bordetella avium with those of B. bronchiseptica, B. pertussis, and B. parapertussis reveals extensive diversity in surface structures associated with host interaction Sebaihia M, Preston A, Maskell DJ, Kuzmiak H, Connell TD, King ND, Orndorff PE, Miyamoto DM, Thomson NR and Temple LM <10 more author(s)> Sebaihia M, Preston A, Maskell DJ, Kuzmiak H, Connell TD, King ND, Orndorff PE, Miyamoto DM, Thomson NR, Harris D, Goble A, Lord A, Murphy L, Quail MA, Rutter S, Squares R, Squares S, Woodward J, Parkhill J, Temple LM (- 10) Ref: Journal of Bacteriology, 188:6002, 2006 : PubMed ESTHER: Sebaihia_2006_J.Bacteriol_188_6002 PubMedSearch: Sebaihia 2006 J.Bacteriol 188 6002 PubMedID: 16885469 Gene_locus related to this paper: bora1-q2kti1, bora1-q2ktw2, bora1-q2ku63, bora1-q2kun8, bora1-q2kuu7, bora1-q2kuz2, bora1-q2kv84, bora1-q2kvg3, bora1-q2kw07, bora1-q2kw58, bora1-q2kwy4, bora1-q2kxl0, bora1-q2kxn8, bora1-q2kxw5, bora1-q2kxz8, bora1-q2kyw6, bora1-q2kzr8, bora1-q2kzt4, bora1-q2kzx4, bora1-q2l0h1, bora1-q2l0h9, bora1-q2l0p4, bora1-q2l1n9, bora1-q2l1v4, bora1-q2l1z1, bora1-q2l122, bora1-q2l209 Abstract Bordetella avium is a pathogen of poultry and is phylogenetically distinct from Bordetella bronchiseptica, Bordetella pertussis, and Bordetella parapertussis, which are other species in the Bordetella genus that infect mammals. In order to understand the evolutionary relatedness of Bordetella species and further the understanding of pathogenesis, we obtained the complete genome sequence of B. avium strain 197N, a pathogenic strain that has been extensively studied. With 3,732,255 base pairs of DNA and 3,417 predicted coding sequences, it has the smallest genome and gene complement of the sequenced bordetellae. In this study, the presence or absence of previously reported virulence factors from B. avium was confirmed, and the genetic bases for growth characteristics were elucidated. Over 1,100 genes present in B. avium but not in B. bronchiseptica were identified, and most were predicted to encode surface or secreted proteins that are likely to define an organism adapted to the avian rather than the mammalian respiratory tracts. These include genes coding for the synthesis of a polysaccharide capsule, hemagglutinins, a type I secretion system adjacent to two very large genes for secreted proteins, and unique genes for both lipopolysaccharide and fimbrial biogenesis. Three apparently complete prophages are also present. The BvgAS virulence regulatory system appears to have polymorphisms at a poly(C) tract that is involved in phase variation in other bordetellae. A number of putative iron-regulated outer membrane proteins were predicted from the sequence, and this regulation was confirmed experimentally for five of these. Title: A comprehensive survey of the Plasmodium life cycle by genomic, transcriptomic, and proteomic analyses Hall N, Karras M, Raine JD, Carlton JM, Kooij TW, Berriman M, Florens L, Janssen CS, Pain A and Sinden RE <20 more author(s)> Hall N, Karras M, Raine JD, Carlton JM, Kooij TW, Berriman M, Florens L, Janssen CS, Pain A, Christophides GK, James K, Rutherford K, Harris B, Harris D, Churcher C, Quail MA, Ormond D, Doggett J, Trueman HE, Mendoza J, Bidwell SL, Rajandream MA, Carucci DJ, Yates JR, 3rd, Kafatos FC, Janse CJ, Barrell B, Turner CM, Waters AP, Sinden RE (- 20) Ref: Science, 307:82, 2005 : PubMed ESTHER: Hall_2005_Science_307_82 PubMedSearch: Hall 2005 Science 307 82 PubMedID: 15637271 Gene_locus related to this paper: plaba-q4ymx5, plaba-q4ysr8, plaba-q4ytp7, plaba-q4yy11, plaba-q4z0q9, plaba-q4z5y0, plaba-q4z5z8, plaba-q4z215, plach-q4x817, plach-q4xb56, plach-q4xbi1, plach-q4xd64, plach-q4xfc7, plach-q4xm16, plach-q4xmx8, plach-q4xmy0, plach-q4xsf9, plach-q4xsg4, plach-q4xsw6, plach-q4xvc8, plach-q4xxw0, plach-q4xxy1, plach-q4y0k9, plach-q4y5u9, plach-q4y6j0, plach-q4y638, plach-q4y740, playo-PY05572, playo-q7rq09 Abstract Plasmodium berghei and Plasmodium chabaudi are widely used model malaria species. Comparison of their genomes, integrated with proteomic and microarray data, with the genomes of Plasmodium falciparum and Plasmodium yoelii revealed a conserved core of 4500 Plasmodium genes in the central regions of the 14 chromosomes and highlighted genes evolving rapidly because of stage-specific selective pressures. Four strategies for gene expression are apparent during the parasites' life cycle: (i) housekeeping; (ii) host-related; (iii) strategy-specific related to invasion, asexual replication, and sexual development; and (iv) stage-specific. We observed posttranscriptional gene silencing through translational repression of messenger RNA during sexual development, and a 47-base 3' untranslated region motif is implicated in this process. Title: The genome of the kinetoplastid parasite, Leishmania major Ivens AC, Peacock CS, Worthey EA, Murphy L, Aggarwal G, Berriman M, Sisk E, Rajandream MA, Adlem E and Myler PJ <91 more author(s)> Ivens AC, Peacock CS, Worthey EA, Murphy L, Aggarwal G, Berriman M, Sisk E, Rajandream MA, Adlem E, Aert R, Anupama A, Apostolou Z, Attipoe P, Bason N, Bauser C, Beck A, Beverley SM, Bianchettin G, Borzym K, Bothe G, Bruschi CV, Collins M, Cadag E, Ciarloni L, Clayton C, Coulson RM, Cronin A, Cruz AK, Davies RM, De Gaudenzi J, Dobson DE, Duesterhoeft A, Fazelina G, Fosker N, Frasch AC, Fraser A, Fuchs M, Gabel C, Goble A, Goffeau A, Harris D, Hertz-Fowler C, Hilbert H, Horn D, Huang Y, Klages S, Knights A, Kube M, Larke N, Litvin L, Lord A, Louie T, Marra M, Masuy D, Matthews K, Michaeli S, Mottram JC, Muller-Auer S, Munden H, Nelson S, Norbertczak H, Oliver K, O'Neil S, Pentony M, Pohl TM, Price C, Purnelle B, Quail MA, Rabbinowitsch E, Reinhardt R, Rieger M, Rinta J, Robben J, Robertson L, Ruiz JC, Rutter S, Saunders D, Schafer M, Schein J, Schwartz DC, Seeger K, Seyler A, Sharp S, Shin H, Sivam D, Squares R, Squares S, Tosato V, Vogt C, Volckaert G, Wambutt R, Warren T, Wedler H, Woodward J, Zhou S, Zimmermann W, Smith DF, Blackwell JM, Stuart KD, Barrell B, Myler PJ (- 91) Ref: Science, 309:436, 2005 : PubMed ESTHER: Ivens_2005_Science_309_436 PubMedSearch: Ivens 2005 Science 309 436 PubMedID: 16020728 Gene_locus related to this paper: leima-e9ady6, leima-L2464.12, leima-L2802.02, leima-OPB, leima-q4fw33, leima-q4fwg8, leima-q4fwj0, leima-q4fya7, leima-q4q0a1, leima-q4q0t5, leima-q4q0v0, leima-q4q1h9, leima-q4q2c9, leima-q4q4j7, leima-q4q4t6, leima-q4q5j1, leima-q4q6e9, leima-q4q7v8, leima-q4q8a8, leima-q4q9g9, leima-q4q080, leima-q4q398, leima-q4q615, leima-q4q819, leima-q4q871, leima-q4q942, leima-q4qae7, leima-q4qb85, leima-q4qdz7, leima-q4qe26, leima-q4qe31, leima-q4qe85, leima-q4qe86, leima-q4qe87, leima-q4qe90, leima-q4qec8, leima-q4qgz4, leima-q4qgz5, leima-q4qhs0, leima-q4qj45 Abstract Leishmania species cause a spectrum of human diseases in tropical and subtropical regions of the world. We have sequenced the 36 chromosomes of the 32.8-megabase haploid genome of Leishmania major (Friedlin strain) and predict 911 RNA genes, 39 pseudogenes, and 8272 protein-coding genes, of which 36% can be ascribed a putative function. These include genes involved in host-pathogen interactions, such as proteolytic enzymes, and extensive machinery for synthesis of complex surface glycoconjugates. The organization of protein-coding genes into long, strand-specific, polycistronic clusters and lack of general transcription factors in the L. major, Trypanosoma brucei, and Trypanosoma cruzi (Tritryp) genomes suggest that the mechanisms regulating RNA polymerase II-directed transcription are distinct from those operating in other eukaryotes, although the trypanosomatids appear capable of chromatin remodeling. Abundant RNA-binding proteins are encoded in the Tritryp genomes, consistent with active posttranscriptional regulation of gene expression. 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: Genomic sequence of the pathogenic and allergenic filamentous fungus Aspergillus fumigatus Nierman WC, Pain A, Anderson MJ, Wortman JR, Kim HS, Arroyo J, Berriman M, Abe K, Archer DB and Denning DW <87 more author(s)> Nierman WC, Pain A, Anderson MJ, Wortman JR, Kim HS, Arroyo J, Berriman M, Abe K, Archer DB, Bermejo C, Bennett J, Bowyer P, Chen D, Collins M, Coulsen R, Davies R, Dyer PS, Farman M, Fedorova N, Feldblyum TV, Fischer R, Fosker N, Fraser A, Garcia JL, Garcia MJ, Goble A, Goldman GH, Gomi K, Griffith-Jones S, Gwilliam R, Haas B, Haas H, Harris D, Horiuchi H, Huang J, Humphray S, Jimenez J, Keller N, Khouri H, Kitamoto K, Kobayashi T, Konzack S, Kulkarni R, Kumagai T, Lafon A, Latge JP, Li W, Lord A, Lu C, Majoros WH, May GS, Miller BL, Mohamoud Y, Molina M, Monod M, Mouyna I, Mulligan S, Murphy L, O'Neil S, Paulsen I, Penalva MA, Pertea M, Price C, Pritchard BL, Quail MA, Rabbinowitsch E, Rawlins N, Rajandream MA, Reichard U, Renauld H, Robson GD, Rodriguez de Cordoba S, Rodriguez-Pena JM, Ronning CM, Rutter S, Salzberg SL, Sanchez M, Sanchez-Ferrero JC, Saunders D, Seeger K, Squares R, Squares S, Takeuchi M, Tekaia F, Turner G, Vazquez de Aldana CR, Weidman J, White O, Woodward J, Yu JH, Fraser C, Galagan JE, Asai K, Machida M, Hall N, Barrell B, Denning DW (- 87) Ref: Nature, 438:1151, 2005 : PubMed ESTHER: Nierman_2005_Nature_438_1151 PubMedSearch: Nierman 2005 Nature 438 1151 PubMedID: 16372009 Gene_locus related to this paper: aspfc-b0xp50, aspfc-b0xu40, aspfc-b0xzj6, aspfc-dpp5, aspfu-apth1, aspfu-axe1, aspfu-CBPYA, aspfu-faec, aspfu-kex1, aspfu-ppme1, aspfu-q4wa39, aspfu-q4wa78, aspfu-q4wf56, aspfu-q4wg73, aspfu-q4wk44, aspfu-q4wkh6, aspfu-q4wnx3, aspfu-q4wpb9, aspfu-q4wqv2, aspfu-q4wub2, aspfu-q4wxr1, aspfu-q4x0n6, aspfu-q4x1n0, aspfu-q5vjg7, neofi-a1cwa6, neofi-a1dfr9, aspfm-a0a084bf80, aspfu-fmac Abstract Aspergillus fumigatus is exceptional among microorganisms in being both a primary and opportunistic pathogen as well as a major allergen. Its conidia production is prolific, and so human respiratory tract exposure is almost constant. A. fumigatus is isolated from human habitats and vegetable compost heaps. In immunocompromised individuals, the incidence of invasive infection can be as high as 50% and the mortality rate is often about 50% (ref. 2). The interaction of A. fumigatus and other airborne fungi with the immune system is increasingly linked to severe asthma and sinusitis. Although the burden of invasive disease caused by A. fumigatus is substantial, the basic biology of the organism is mostly obscure. Here we show the complete 29.4-megabase genome sequence of the clinical isolate Af293, which consists of eight chromosomes containing 9,926 predicted genes. Microarray analysis revealed temperature-dependent expression of distinct sets of genes, as well as 700 A. fumigatus genes not present or significantly diverged in the closely related sexual species Neosartorya fischeri, many of which may have roles in the pathogenicity phenotype. The Af293 genome sequence provides an unparalleled resource for the future understanding of this remarkable fungus. Title: Insight into the genome of Aspergillus fumigatus: analysis of a 922 kb region encompassing the nitrate assimilation gene cluster Pain A, Woodward J, Quail MA, Anderson MJ, Clark R, Collins M, Fosker N, Fraser A, Harris D and Hall N <15 more author(s)> Pain A, Woodward J, Quail MA, Anderson MJ, Clark R, Collins M, Fosker N, Fraser A, Harris D, Larke N, Murphy L, Humphray S, O'Neil S, Pertea M, Price C, Rabbinowitsch E, Rajandream MA, Salzberg S, Saunders D, Seeger K, Sharp S, Warren T, Denning DW, Barrell B, Hall N (- 15) Ref: Fungal Genet Biol, 41:443, 2004 : PubMed ESTHER: Pain_2004_Fungal.Genet.Biol_41_443 PubMedSearch: Pain 2004 Fungal.Genet.Biol 41 443 PubMedID: 14998527 Gene_locus related to this paper: aspfu-q6my76, aspfu-q6myf7, aspfu-q6myz3 Abstract Aspergillus fumigatus is the most ubiquitous opportunistic filamentous fungal pathogen of human. As an initial step toward sequencing the entire genome of A. fumigatus, which is estimated to be approximately 30 Mb in size, we have sequenced a 922 kb region, contained within 16 overlapping bacterial artificial chromosome (BAC) clones. Fifty-four percent of the DNA is predicted to be coding with 341 putative protein coding genes. Functional classification of the proteins showed the presence of a higher proportion of enzymes and membrane transporters when compared to those of Saccharomyces cerevisiae. In addition to the nitrate assimilation gene cluster, the quinate utilisation gene cluster is also present on this 922 kb genomic sequence. We observed large scale synteny between A. fumigatus and Aspergillus nidulans by comparing this sequence to the A. nidulans genetic map of linkage group VIII. 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: 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. | |||||||
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