A Regulator Modulates Intestinal Colonization and Use of Phosphonoacetic Acid.

Many microorganisms produce phosphonates, molecules characterized by stable carbon-phosphorus bonds that store phosphorus or act as antimicrobials. The role of phosphonates in the marine biosphere is well characterized but the role of these molecules in the intestine is poorly understood. uses its virulence factors to influence the host immune response to compete with the host and normal microflora for nutrients. cannot produce phosphonates but encodes the enzymes to use them suggesting that it is exposed to phosphonates during its life cycle. The role of phosphonates during enteric salmonellosis is unexplored. We have previously shown that , encoding a putative regulator of phosphonate metabolism, is needed for colonization in calves. Here, we report that the necessity of in colonization of the murine intestine results from multiple factors. is needed for full activation of the type-3 secretion system-1 and for optimal invasion of epithelial cells. The Δ mutant grows poorly in phosphonoacetic acid (PA) as the sole phosphorus source, but can use 2-aminoethylphosphonate. PhnA, an enzyme required for PA breakdown, is not controlled by STM3602 suggesting an additional mechanism for utilization of PA in . Typhimurium. Finally, the requirement of for intestinal colonization differs depending on the composition of the microflora. Our data suggest that has multiple regulatory targets that are necessary for survival within the microbial community in the intestine. Determination of the members of the regulon may illuminate new pathways needed for colonization of the host.