Regulation of the Expression of Iron-acquisition System Genes in Pathogenic Vibrio Species

Abstract

 The genus Vibrio includes >70 species, of which roughly a dozen cause vibriosis such as gastroenteritis, wound infections, and septicemia. Most bacteria, including Vibrio species, require iron for survival and growth. However, the bioavailability of iron is extremely low because it is usually present as an insoluble ferric complex in an aerobic environment or is bound to iron-binding proteins in mammalian hosts. Therefore many bacteria have developed iron acquisition systems, including biosynthesis and secretion of low-molecular-mass iron-chelating compounds called siderophores, and uptake of iron-bound siderophores into bacterial cells through specific active transport systems. Vibrio parahaemolyticus, a major pathogenic Vibrio species, contains multiple iron-acquisition systems mediated by its own siderophore vibrioferrin and several xenosiderophores produced by other microorganisms. In this review, I have focused on the transcriptional and posttranscriptional regulation of genes encoding iron acquisition systems in V. parahaemolyticus. All genes involved in its iron acquisition systems are repressed by Fur, which acts as a ferrous-dependent transcriptional repressor. Furthermore, the stability of polycistronic mRNA involved in vibrioferrin biosynthesis is positively regulated by a small RNA, RyhB, which is repressed by Fur. Expression of PeuA receptor required for utilization of a xenosiderophore, enterobactin, occurs under iron-limiting conditions at alkaline pH. PeuA expression is induced by a two-component regulatory system, PeuRS, which enhances expression of an alternative peuA transcript without an intrinsic translation-inhibitory structure in response to changes in alkaline pH.