The Small RNA PinT Contributes to PhoP-Mediated Regulation of the Salmonella Pathogenicity Island 1 Type III Secretion System in Salmonella enterica Serovar Typhimurium

• Published in: Journal of bacteriology Vol. 201; no. 19; p. 1
• Main Authors: Kim, Kyungsub, Palmer, Alexander D, Vanderpool, Carin K, Slauch, James M
• Format: Journal Article
• Language: English
• Published: United States American Society for Microbiology 01-10-2019
• Subjects: Bacteriology; Base pairs; Biodegradation; Control; Diarrhea; Environmental regulations; Epithelial cells; Inflammation; Intestine; Intracellular; Macrophages; Pathogenicity; Pathogens; Post-transcription; Regulation; Ribonucleic acid; RNA; Salmonella; Salmonella enterica; Secretion; Survival; Translation; Virulence; PhoPQ; Salmonella; SPI1; sRNA
• ISSN: 0021-9193; 1098-5530
• DOI: 10.1128/JB.00312-19

serovar Typhimurium induces inflammatory diarrhea and bacterial uptake into intestinal epithelial cells using the
pathogenicity island 1 (SPI1) type III secretion system (T3SS). HilA activates transcription of the SPI1 structural components and effector proteins. Expression of
is activated by HilD, HilC, and RtsA, which act in a complex feed-forward regulatory loop. Many environmental signals and other regulators are integrated into this regulatory loop, primarily via HilD. After the invasion of
into host intestinal epithelial cells or during systemic replication in macrophages, the SPI T3SS is no longer required or expressed. We have shown that the two-component regulatory system PhoPQ, required for intracellular survival, represses the SPI1 T3SS mostly by controlling the transcription of
and
Here we show that PinT, one of the PhoPQ-regulated small RNAs (sRNAs), contributes to this regulation by repressing
and
translation. PinT base pairs with both the
and
mRNAs, resulting in translational inhibition of
, but also induces degradation of the
transcript. PinT also indirectly represses expression of FliZ, a posttranslational regulator of HilD, and directly represses translation of
, encoding the primary regulator of the SPI2 T3SS. Our
mouse competition assays support the concept that PinT controls a series of virulence genes at the posttranscriptional level in order to adapt
from the invasion stage to intracellular survival.
is one of the most important food-borne pathogens, infecting over one million people in the United States every year. These bacteria use a needle-like device to interact with intestinal epithelial cells, leading to invasion of the cells and induction of inflammatory diarrhea. A complex regulatory network controls expression of the invasion system in response to numerous environmental signals. Here we explore the molecular mechanisms by which the small RNA PinT contributes to this regulation, facilitating inactivation of the system after invasion. PinT controls several important virulence systems in
, tuning the transition between different stages of infection.