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Bacteria utilize endoribonuclease-mediated RNA processing and decay to rapidly adapt to environmental changes. Here, we report that the modulation of  hns  mRNA stability by the endoribonuclease RNase G plays a key role in  Salmonella  Typhimurium pathogenicity. We found that RNase G determines the half-life of  hns  mRNA by cleaving its 5′ untranslated region and that altering its cleavage sites by genome editing stabilizes  hns  mRNA, thus decreasing  S . Typhimurium virulence in mice. Under anaerobic conditions, the FNR-mediated transcriptional repression of  rnc  encoding RNase III, which degrades  rng  mRNA, and simultaneous induction of  rng  transcription resulted in rapid  hns  mRNA degradation, leading to the derepression of genes involved in the  Salmonella  pathogenicity island 1 (SPI-1) type III secretion system (T3SS). Together, our findings show that RNase III and RNase G levels-mediated control of  hns  mRNA abundance acts as a regulatory pathway upstream of a complex feed-forward loop for SPI-1 expression.

plos pathogens

Endoribonuclease-mediated control of hns mRNA stability constitutes a key regulatory pathway for Salmonella Typhimurium pathogenicity island 1 expression