Salmonella enterica
serovar Typhimurium is a prominent foodborne pathogen, infecting millions of people a year. To express virulence genes at the correct time and place in the host,
Salmonella
uses a complex regulatory network that senses environmental conditions.
Salmonella enterica serovar Typhimurium is an enteric pathogen associated with food-borne disease. Salmonella invades the intestinal epithelium using a type three secretion system encoded in Salmonella pathogenicity Island 1 (SPI-1). SPI-1 genes are tightly regulated by a complex feed-forward loop to ensure proper spatial and temporal expression. The master regulator, HilD, possesses a 310-nucleotide 3′ untranslated region (UTR) that influences hilD and SPI-1 expression. Since this regulatory effect is dependent on Hfq and RNase E, cofactors known to mediate small RNA (sRNA) regulatory activities, we hypothesized that the hilD mRNA 3′ UTR is a target for sRNAs. Here, we show that the sRNAs, SdsR and Spot 42 regulate SPI-1 by targeting different regions of the hilD mRNA 3′ UTR. Regulatory activities of these sRNAs depend on Hfq and RNase E, in agreement with previous roles found for both at the hilD 3′ UTR. We show that SdsR and RNase E are responsible for the accumulation of variable fragments of the hilD mRNA 3′ UTR. Collectively, this work suggests that these sRNAs targeting the hilD mRNA 3′ UTR regulate hilD mRNA levels by interfering with RNase E-dependent mRNA degradation. Our work provides novel insights into mechanisms of sRNA regulation at bacterial mRNA 3′ UTRs and adds to our knowledge of post-transcriptional regulation of the SPI-1 complex feed-forward loop.
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