Thu, 24 Jul 2008 19:53:03 BST CiteULike: Xavier Wagner http://www.citeulike.org/user/Xavier/author/Wagner CiteULike.org en-gb Copyright © 2004-2008 citeulike.org http://www.citeulike.org/user/Xavier/article/2485534 <i>PLoS ONE, Vol. 2, No. 9. (2007)</i><br /><br />Francisella tularensis is the causative agent of tularemia, which is a highly lethal disease from nature and potentially from a biological weapon. This species contains four recognized subspecies including the North American endemic F. tularensis subsp. tularensis (type A), whose genetic diversity is correlated with its geographic distribution including a major population subdivision referred to as A.I and A.II. The biological significance of the A.I - A.II genetic differentiation is unknown, though there are suggestive ecological and epidemiological correlations. In order to understand the differentiation at the genomic level, we have determined the complete sequence of an A.II strain (WY96-3418) and compared it to the genome of Schu S4 from the A.I population. We find that this A.II genome is 1,898,476 bp in size with 1,820 genes, 1,303 of which code for proteins. While extensive genomic variation exists between "WY96" and Schu S4, there is only one whole gene difference. This one gene difference is a hypothetical protein of unknown function. In contrast, there are numerous SNPs (3,367), small indels (1,015), IS element differences (7) and large chromosomal rearrangements (31), including both inversions and translocations. The rearrangement borders are frequently associated with IS elements, which would facilitate intragenomic recombination events. The pathogenicity island duplicated regions (DR1 and DR2) are essentially identical in WY96 but vary relative to Schu S4 at 60 nucleotide positions. Other potential virulence-associated genes (231) varied at 559 nucleotide positions, including 357 non-synonymous changes. Molecular clock estimates for the divergence time between A.I and A.II genomes for different chromosomal regions ranged from 866 to 2131 years before present. This paper is the first complete genomic characterization of a member of the A.II clade of Francisella tularensis subsp. tularensis. Complete Genomic Characterization of a Pathogenic A.II Strain of Francisella tularensis Subspecies tularensis. SM Beckstrom-Sternberg RK Auerbach S Godbole JV Pearson JS Beckstrom-Sternberg Z Deng C Munk K Kubota Y Zhou D Bruce J Noronha RH Scheuermann A Wang X Wei J Wang J Hao DM Wagner TS Brettin N Brown P Gilna PS Keim doi:10.1371/journal.pone.0000947 PLoS ONE, Vol. 2, No. 9. (2007) 2008-03-07T16:29:56-00:00 2007 PLoS ONE 1932-6203 2 9 frank http://www.citeulike.org/user/Xavier/article/2461427 <i>Proc Natl Acad Sci U S A, Vol. 103, No. 34. (22 August 2006), pp. 12879-12884.</i><br /><br />Uropathogenic Escherichia coli (UPEC) strain 536 (O6:K15:H31) is one of the model organisms of extraintestinal pathogenic E. coli (ExPEC). To analyze this strain's genetic basis of urovirulence, we sequenced the entire genome and compared the data with the genome sequence of UPEC strain CFT073 (O6:K2:H1) and to the available genomes of nonpathogenic E. coli strain MG1655 (K-12) and enterohemorrhagic E. coli. The genome of strain 536 is approximately 292 kb smaller than that of strain CFT073. Genomic differences between both UPEC are mainly restricted to large pathogenicity islands, parts of which are unique to strain 536 or CFT073. Genome comparison underlines that repeated insertions and deletions in certain parts of the genome contribute to genome evolution. Furthermore, 427 and 432 genes are only present in strain 536 or in both UPEC, respectively. The majority of the latter genes is encoded within smaller horizontally acquired DNA regions scattered all over the genome. Several of these genes are involved in increasing the pathogens' fitness and adaptability. Analysis of virulence-associated traits expressed in the two UPEC O6 strains, together with genome comparison, demonstrate the marked genetic and phenotypic variability among UPEC. The ability to accumulate and express a variety of virulence-associated genes distinguishes ExPEC from many commensals and forms the basis for the individual virulence potential of ExPEC. Accordingly, instead of a common virulence mechanism, different ways exist among ExPEC to cause disease. How to become a uropathogen: comparative genomic analysis of extraintestinal pathogenic Escherichia coli strains. E Brzuszkiewicz H Brüggemann H Liesegang M Emmerth T Olschläger G Nagy K Albermann C Wagner C Buchrieser L Emody G Gottschalk J Hacker U Dobrindt doi:10.1073/pnas.0603038103 Proc Natl Acad Sci U S A, Vol. 103, No. 34. (22 August 2006), pp. 12879-12884. 2008-03-03T18:21:45-00:00 2006 Proc Natl Acad Sci U S A 0027-8424 103 34 12879 12884 coli