Yersinia pseudotuberculosis YPIII
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA239223 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1175460_1.fastq.gz | Fastqsanger.gz | |||
| SRR1175460_2.fastq.gz | Fastqsanger.gz | |||
| SRR1175461_1.fastq.gz | Fastqsanger.gz | |||
| SRR1175461_2.fastq.gz | Fastqsanger.gz | |||
| SRR1175462_1.fastq.gz | Fastqsanger.gz |
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Project description:Expression of the virulence regulator RovA of Yersinia pseudotuberculosis, is controlled by the ncRNAs CsrB and CsrC through CsrA and RovM. In this study, we show that the regulator YmoA of the Hha family of nucleoid-associated proteins controls expression of the counterregulated Csr-type RNAs and the Csr-RovM-RovA signalling cascade through alterations of the CsrC RNA stability. YmoA-mediated stabilization of CsrC depends on CsrA and H-NS, but not on the RNA chaperone Hfq and involves a stabilizing stem-loop structure within the 5’-region of CsrC. YmoA influence on CsrC stability is complex as YmoA was found to control numerous factors known to affect RNA structures and stability. In addition, YmoA controls temperature-dependent early and later stage virulence genes in an opposite manner and coregulates their expression with bacterial stress responses and metabolic functions. Following oral infections in a mouse model, we demonstrate that a ymoA mutant is strongly reduced in its ability to disseminate to the Peyer’s patches, mesenteric lymph nodes, liver and spleen and exhibits a reduced mortality. We propose a model in which YmoA controls switching from a RovA-dependent early colonization phase towards a virulence plasmid (pYV)-dependent infection phase important for host defense and persistence.
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Project description:Yersinia pseudotuberculosis YPIII Genome sequencing
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Project description:Expression of the virulence regulator RovA of Yersinia pseudotuberculosis, is controlled by the ncRNAs CsrB and CsrC through CsrA and RovM. In this study, we show that the regulator YmoA of the Hha family of nucleoid-associated proteins controls expression of the counterregulated Csr-type RNAs and the Csr-RovM-RovA signalling cascade through alterations of the CsrC RNA stability. YmoA-mediated stabilization of CsrC depends on CsrA and H-NS, but not on the RNA chaperone Hfq and involves a stabilizing stem-loop structure within the 5M-bM-^@M-^Y-region of CsrC. YmoA influence on CsrC stability is complex as YmoA was found to control numerous factors known to affect RNA structures and stability. In addition, YmoA controls temperature-dependent early and later stage virulence genes in an opposite manner and coregulates their expression with bacterial stress responses and metabolic functions. Following oral infections in a mouse model, we demonstrate that a ymoA mutant is strongly reduced in its ability to disseminate to the PeyerM-bM-^@M-^Ys patches, mesenteric lymph nodes, liver and spleen and exhibits a reduced mortality. We propose a model in which YmoA controls switching from a RovA-dependent early colonization phase towards a virulence plasmid (pYV)-dependent infection phase important for host defense and persistence. For each microarray, 300ng of each Cy3- and Cy5-labelled RNA were mixed, fragmented and hybridized to the microarray at 65M-BM-0C for 17 hours using the Agilent Hybridization Chamber according to the Agilent instructions. Four replicates were performed. Sequences used for the design of the microarray (Agilent, 8 x 15K format) include three different 60-nt oligonucleotides for all 4172 chromosomal genes (ORFs > 30 codons) of the Y. pseudotuberculosis YPIII genome and six probes for the 92 genes of the virulence plasmid pYV of Y. pseudotuberculosis strain IP32953.
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Project description:Yersinia pseudotuberculosis is a Gram-negative bacterium capable of causing gastrointestinal infection and is closely related to the highly virulent plague bacillus Yersinia pestis. Infection by both species are currently treatable with antibiotics such as ciprofloxacin, a quinolone-class drug of major clinical importance in the treatment of many other infections. Our current understanding of the mechanism of action of ciprofloxacin is that it inhibits DNA replication by targeting DNA gyrase, and that resistance is primarily due to mutation at this target site, along with generic efflux and detoxification strategies. We utilised transposon directed insertion site sequencing (TraDIS or TnSeq) to identify the non-essential chromosomal genes in Y. pseudotuberculosis that are required to tolerate sub-lethal concentrations of ciprofloxacin in vitro. As well as highlighting recognised antibiotic resistance genes, we provide evidence that a multitude of genes involved in regulating DNA replication and repair are central in enabling Y. pseudotuberculosis to tolerate the antibiotic, including dksA (yptb0734), a regulator of RNA polymerase and hda (yptb2792), an inhibitor of DNA replication initiation. We furthermore demonstrate that even at sub-lethal concentrations, ciprofloxacin causes severe cell-wall stress, requiring lipopolysaccharide lipid A, O-antigen and core biosynthesis genes to resist the sub-lethal effects of the antibiotic. It is evident that coping with the consequence(s) of antibiotic-induced stress requires the contribution of scores of genes that are not exclusively engaged in drug-resistance.
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