In vitroandin vivoinfection models reveal connection between periplasmic protease Prc and alternative peptidoglycan synthase PBP3SALinSalmonella entericaserovar Typhimurium

Abstract

AbstractA hallmark in salmonellosis is the ability of the bacteria to proliferate within host cells. Most notably,Salmonellaproliferates within professional phagocytes in a vacuolar compartment. During proliferationSalmonellahas to build new cell wall, but how this is regulated within the intraphagosomal niche is not known. Here we show that genetically inactivating the periplasmic protease Prc, involved in cleaving peptidoglycan-processing enzymes, results in decreased fitness in macrophage-like RAW264.7 cells and in BALB/c mice, and in a decreased tolerance to redox stress. All theseprcmutant phenotypes were conditional depending onpbp3sal, a recently defined paralogue forftslcoding for the essential penicillin binding protein 3. These phenotypic connections between Prc and PBP3SALadds to the phenotypes governed by Prc, and possibly adds PBP3SALto the pool of target proteins involved in cell wall homeostasis that are regulated by Prc.