RpoN is required for a functional type III secretion system in Yersinia pseudotuberculosis

Abstract

AbstractPathogenic bacteria use a broad range of virulence factors to thrive within their host. Yersinia pseudotuberculosis, a gram-negative enteropathogen in humans, utilises a Type III secretion system to overcome the host’s innate immune response. A global regulator previously shown to be essential for virulence in Y. pseudotuberculosis is RpoN. We show here that a strain lacking RpoN has a severely reduced capacity to secrete Yop effectors. This strain has a substantially reduced expression of genes encoding structural components of the secretion apparatus, the ysc operons, while expression of genes encoding effectors and translocators is less affected. We show that RpoN regulates a complex network, where one part is suggested to contribute to inducing Type III secretion via the enhancer-binding protein GlrR/RpoN regulon. By analogy, during inducement of Type III secretion, RpoN has a positive effect on expression of the sigma factor RpoE, which also is known to act downstream of GlrR. Interestingly, we found putative RpoE binding sites upstream of the ysc operons, and also a partial rescue of Yop secretion in the rpoN mutant strain by overexpression of RpoE. Our findings suggest that the RpoN-mediated effect on expression of type III genes involves a sigma factor hierarchy, where RpoN via RpoE contributes to inducing Type III secretion.