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A 3’UTR-derived small RNA modulates the life-cycle of the cholera toxin-encoding filamentous phage, CTXϕ [RNA-Seq]

ABSTRACT: Bacteriophages (phages) are well known to be one of the major driving forces in bacterial evolution. This is also true for virulent microorganisms, such as the major human pathogen Vibrio cholerae, whose pathogenic potential and epidemic proliferation largely depends on the interaction with environmental phages. Specifically, integration of the CTXϕ phage genome into the first chromosome of V. cholerae also involved the ctxAB genes, encoding the principle toxin responsible for the severe acute diarrheal disease, cholera. Whereas the mechanisms underlying CTXϕ-associated horizontal gene transfer and control of the ctxAB genes have been intensively studied over the past years, post-transcriptional regulation affecting the CTXϕ lifecycle has not been documented. Here, we report the discovery and characterization of the CisR small RNA (sRNA) that is produced from the 3’UTR (untranslated region) of the prtV gene and inhibits the expression of the CTXϕ-encoded cep mRNA. CisR-mediated repression of cep involves Hfq-assisted base-pairing of the two transcripts and results in reduced CTXϕ production under stress conditions. We further show that transcription of prtV-cisR requires both, the master quorum sensing transcription factor HapR, as well CRP, which coordinates global carbon metabolism. Taken together, our work provides evidence that V. cholerae employs sRNA-mediated post-transcriptional gene regulation to coordinate CTXϕ activation with both cell density and nutrient availability.

ORGANISM(S): Vibrio cholerae

PROVIDER: GSE311502 | GEO | 2025/12/03

REPOSITORIES: GEO

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Project description:Cholera is a diarrheal disease caused by Vibrio cholerae of serogroups O1 and O139 that affects impoverished populations worldwide. The histone-like nucleoid structuring protein (H-NS) is a global regulator of environmentally-regulated gene expression that plays a fundamental role in V. cholerae adaptation to disparate ecological niches. We used RNA-seq to characterize the hns transcriptome of El Tor biotype V. cholerae. H-NS affected the expression of 18% of all predicted genes in a growth phase-dependent manner. It silenced the transcription of genes encoding virulence regulators and cytotoxic factors such as the VieSAB regulatory system, the repeat in toxin (RTX) and hemolysin. H-NS was 10 times more effective in silencing the vieSAB promoter in El Tor compared to classical biotype V. cholerae. In the El Tor biotype hns mutant, VieSAB significantly enhanced the expression of cholera toxin genes. For the RTX and hemolysin, we found that overexpression of the transcription activator HlyU diminished H-NS occupancy at the hlyA promoter but not at the rtxCA and rtxBDE promoters. H-NS had a significant impact on the cell envelope and the mutant expressed elevated rpoE encoding the extracytoplamic sigma factor E (sE), though this effect was indirect. A remarkable feature of the hns transcriptome was the down-regulation of numerous methyl-accepting chemotaxis proteins in early stationary phase that translated into diminished chemotaxis toward the amino acids glycine and serine. Our study suggests that H-NS transcriptional silencing can contribute to multiple phenotypic differences observed between V. cholerae biotypes, mainly by differentially repressing the VieSAB sensory pathway. Transcriptome profiles of wild type and M-NM-^Thns mutant cells of the V. cholerae strain C7258 grown in LB medium were generated by Next Generation Sequencing using the Illumina HiSeq2000 platform. Samples from mid-exponential phase (OD600 0.5) and early stationary phase (OD600 2.0) were analyzed in duplicate

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A 3’UTR-derived small RNA modulates the life-cycle of the cholera toxin-encoding filamentous phage, CTXϕ [RNA-Seq]

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