Report

pH Sensing by Intracellular Salmonella Induces Effector Translocation

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Science  15 Apr 2010:
1189000
DOI: 10.1126/science.1189000

Abstract

Salmonella enterica is an important intracellular bacterial pathogen of humans and animals. It replicates within host cell vacuoles by delivering virulence (effector) proteins through a vacuolar membrane pore made by the SPI-2 type III secretion system (T3SS). T3SS assembly follows vacuole acidification, but when bacteria are grown at low pH, effector secretion is negligible. Here, we found that effector secretion was activated at low pH from mutant strains lacking a complex of SPI-2–encoded proteins SsaM, SpiC, and SsaL. Exposure of wild-type bacteria to pH 7.2 after growth at pH 5.0 caused dissociation and degradation of SsaM/SpiC/SsaL complexes and effector secretion. In infected cells, loss of the pH 7.2 signal by acidification of host cell cytosol prevented complex degradation and effector translocation. Thus, intravacuolar Salmonella senses host cytosolic pH, resulting in degradation of regulatory complex proteins and effector translocation.