Characterization of the Listeria monocytogenes PieRS regulon distinguishes the function of the critical secretion chaperone PrsA2 from other regulon members.

Abstract

Listeria monocytogenes (Lm) is a gram-positive pathogen that is widespread throughout the environment and known for its ability to infect mammalian hosts following the ingestion of contaminated food. Lm uses a variety of mechanisms to survive challenging conditions experienced both during life in the outside environment and inside of the infected host. We recently described a novel two-component signaling system known as PieRS that regulates the secretion of the chaperone PrsA2, which is essential for bacterial virulence, as well as its related homolog PrsA1 and a variety of gene products of unknown function. Here, we examine the roles of the less characterized PieRS-regulated gene products and contrast their functions with PrsA2 in terms of bacterial survival under stress conditions and virulence in mice. Characterization of targeted in-frame deletion mutants of PieRS regulon members indicates-in contrast to prsA2 mutants-minimal contributions to stress survival and bacterial virulence. Modest contributions of select regulon members were associated with Lm colonization of the gastrointestinal tract. The PieRS regulon thus consists of gene products that contribute to Lm physiology in ways that are clearly distinct from PrsA2 and the chaperone's essential function for both stress survival and bacterial virulence.