CRP-cAMP mediates silencing of Salmonella virulence at the post-transcriptional level

dc.contributor.authorEl Mouali, Youssef
dc.contributor.authorGaviria-Cantin, Tania
dc.contributor.authorSánchez-Romero, María Antonia
dc.contributor.authorGibert, Marta
dc.contributor.authorWestermann, Alexander J.
dc.contributor.authorVogel, Jörg
dc.contributor.authorBalsalobre, Carlos
dc.date.accessioned2019-08-12T02:26:12Z
dc.date.available2019-08-12T02:26:12Z
dc.date.issued2018
dc.description.abstractInvasion of epithelial cells by Salmonella enterica requires expression of genes located in the pathogenicity island I (SPI-1). The expression of SPI-1 genes is very tightly regulated and activated only under specific conditions. Most studies have focused on the regulatory pathways that induce SPI-1 expression. Here, we describe a new regulatory circuit involving CRP-cAMP, a widely established metabolic regulator, in silencing of SPI-1 genes under non-permissive conditions. In CRP-cAMP-deficient strains we detected a strong upregulation of SPI-1 genes in the mid-logarithmic growth phase. Genetic analyses revealed that CRP-cAMP modulates the level of HilD, the master regulator of Salmonella invasion. This regulation occurs at the post-transcriptional level and requires the presence of a newly identified regulatory motif within the hilD 3’UTR. We further demonstrate that in Salmonella the Hfq-dependent sRNA Spot 42 is under the transcriptional repression of CRP-cAMP and, when this transcriptional repression is relieved, Spot 42 exerts a positive effect on hilD expression. In vivo and in vitro assays indicate that Spot 42 targets, through its unstructured region III, the 3’UTR of the hilD transcript. Together, our results highlight the biological relevance of the hilD 3’UTR as a hub for post-transcriptional control of Salmonella invasion gene expression.en_US
dc.identifier.issn1553-7390
dc.identifier.urihttps://repositorio.usc.edu.co/handle/20.500.12421/545
dc.language.isoenen_US
dc.publisherPLoS Geneticsen_US
dc.titleCRP-cAMP mediates silencing of Salmonella virulence at the post-transcriptional levelen_US
dc.typeArticleen_US

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