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In vivo mRNA profiling of uropathogenic Escherichia coli from diverse phylogroups reveals common and group-specific gene expression profiles.

Bielecki P, Muthukumarasamy U, Eckweiler D, Bielecka A, Pohl S, Schanz A, Niemeyer U, Oumeraci T, von Neuhoff N, Ghigo JM, Häussler S - MBio (2014)

Bottom Line: Furthermore, genes transcribed in vivo relative to laboratory media included well-described virulence factors, small regulatory RNAs, as well as genes not previously linked to bacterial virulence.Knowledge on relevant transcriptional responses that drive pathogenicity and adaptation of isolates to the human host might lead to the introduction of a virulence typing strategy into clinical microbiology, potentially facilitating management and prevention of the disease.This work was undertaken to identify key players in physiological adaptation processes and, hence, potential targets for new infection prevention and therapy interventions specifically aimed at sabotaging bacterial adaptation to the human host.

View Article: PubMed Central - PubMed

Affiliation: Institute for Molecular Bacteriology, Twincore, Centre for Clinical and Experimental Infection Research, A Joint Venture of the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, Germany.

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Phylogenetic tree of 54 previously sequenced strains and the 21 clinical isolates from this (in italic) work based on sequence variation within 336 genes. Phylogenetic groups are indicated based on previous reports (34, 35). The numbers show the bootstrapping values as provided by RaxML.
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fig1: Phylogenetic tree of 54 previously sequenced strains and the 21 clinical isolates from this (in italic) work based on sequence variation within 336 genes. Phylogenetic groups are indicated based on previous reports (34, 35). The numbers show the bootstrapping values as provided by RaxML.

Mentions: In E. coli, <3% of nucleotide divergence is found among conserved genes in the various genomes (6). This high degree of homogeneity allows the establishment of phylograms that are built upon sequence variations. Previous studies have identified five major phylogenetic groups, (B2, B1, D, A, and E), corresponding to E. coli strains with distinct capability to cause disease and to inhabit various ecological niches (31–36). Figure 1 depicts the phylogenetic distribution of previously sequenced E. coli isolates that have been grouped into the five phylogenetic E. coli groups. This tree is based on sequence variations of 336 genes (for those genes, at least 80% sequencing coverage across the 21 UTI isolates was detected), which allowed us to use the genotype information from the RNA-seq data of the E. coli genomes to assign the 21 UTI isolates of this study to the clusters within the phylogenetic tree (Fig. 1). Reflecting the fact that our study group consisted mostly of elderly patients, we found a broad distribution of the 21 UTI-associated isolates between the phylogenetic groups. A total of 43% of the 21 isolates belong to the virulent E. coli strain phylogroups B2 and D (B2, 33%; D, 10%), whereas the others are distributed in the B1 (38%) and A (19%) phylogroups.


In vivo mRNA profiling of uropathogenic Escherichia coli from diverse phylogroups reveals common and group-specific gene expression profiles.

Bielecki P, Muthukumarasamy U, Eckweiler D, Bielecka A, Pohl S, Schanz A, Niemeyer U, Oumeraci T, von Neuhoff N, Ghigo JM, Häussler S - MBio (2014)

Phylogenetic tree of 54 previously sequenced strains and the 21 clinical isolates from this (in italic) work based on sequence variation within 336 genes. Phylogenetic groups are indicated based on previous reports (34, 35). The numbers show the bootstrapping values as provided by RaxML.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4128348&req=5

fig1: Phylogenetic tree of 54 previously sequenced strains and the 21 clinical isolates from this (in italic) work based on sequence variation within 336 genes. Phylogenetic groups are indicated based on previous reports (34, 35). The numbers show the bootstrapping values as provided by RaxML.
Mentions: In E. coli, <3% of nucleotide divergence is found among conserved genes in the various genomes (6). This high degree of homogeneity allows the establishment of phylograms that are built upon sequence variations. Previous studies have identified five major phylogenetic groups, (B2, B1, D, A, and E), corresponding to E. coli strains with distinct capability to cause disease and to inhabit various ecological niches (31–36). Figure 1 depicts the phylogenetic distribution of previously sequenced E. coli isolates that have been grouped into the five phylogenetic E. coli groups. This tree is based on sequence variations of 336 genes (for those genes, at least 80% sequencing coverage across the 21 UTI isolates was detected), which allowed us to use the genotype information from the RNA-seq data of the E. coli genomes to assign the 21 UTI isolates of this study to the clusters within the phylogenetic tree (Fig. 1). Reflecting the fact that our study group consisted mostly of elderly patients, we found a broad distribution of the 21 UTI-associated isolates between the phylogenetic groups. A total of 43% of the 21 isolates belong to the virulent E. coli strain phylogroups B2 and D (B2, 33%; D, 10%), whereas the others are distributed in the B1 (38%) and A (19%) phylogroups.

Bottom Line: Furthermore, genes transcribed in vivo relative to laboratory media included well-described virulence factors, small regulatory RNAs, as well as genes not previously linked to bacterial virulence.Knowledge on relevant transcriptional responses that drive pathogenicity and adaptation of isolates to the human host might lead to the introduction of a virulence typing strategy into clinical microbiology, potentially facilitating management and prevention of the disease.This work was undertaken to identify key players in physiological adaptation processes and, hence, potential targets for new infection prevention and therapy interventions specifically aimed at sabotaging bacterial adaptation to the human host.

View Article: PubMed Central - PubMed

Affiliation: Institute for Molecular Bacteriology, Twincore, Centre for Clinical and Experimental Infection Research, A Joint Venture of the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, Germany.

Show MeSH
Related in: MedlinePlus