RcsB-dependent regulation of type VI secretion system in porcine extra-intestinal pathogenic Escherichia coli.

Abstract

Signal transduction system and specialized secretory devices are crucial for bacteria to sense and adequately adapt in adverse environmental conditions. Therefore, it's crucial for microbes to detect and respond to lethal attacks when envelope is perturbed so as to minimize and fix the damage in milieu. We investigated the adaptive response of porcine extra-intestinal pathogenic Escherichia coli PCN033 to polymyxin B challenge. Treatment with polymyxin B led to rapid and robust activation of Rcs system via RcsF, as well as the accumulation of reactive oxygen species. ExPEC T6SS expression was strongly induced by RcsB in Rcs system, resulting in the reduction in the damage to constitute a survival strategy. Finally, we show that T6SS of ExPEC is involved in its pathogenicity in mouse model. Compared with the wild type strain, the deletion of T6SS genes led to a decrease in the organ colonization ability, and the RcsFS2DM3Q mutant that caused Rcs activation had a stronger colonization ability than the wild type strain. In conclusion, Rcs system orchestrates Rcs cascade to trigger antioxidant defense of T6SS, and presents a typical model in which a bacterium reschedule its transcription network via the Rcs phosphorelay pathway in response to membrane perturbations for survival and pathogenesis.