Edwardsiella piscicida requires SecY homeostasis facilitated by FtsH and YccA for stress resistance and virulence

Abstract

Edwardsiella piscicida is a frequent fish pathogen that brings about huge economic losses in the aquaculture industry. Bacterial protein secretion is prominent for bacterial survival and virulence. SecY is the central subunit of Sec translocon and plays a vital role in protein secretion. However, the role of SecY in pathogenicity remains totally unknown in E. piscicida. In current study, we demonstrate that the decrease of SecY expression level in E. piscicida impairs bacterial stress tolerance including oxidative stress, high-temperature stress, antibiotic stress, and host serum stress, and weakens bacterial pathogenicity including adhesion to non-phagocyte, proliferation in phagocyte, dissemination in immune tissue, and the overall virulence. The SecY level increases in the absence of metalloproteinase FtsH and decrease in the absence of transmembrane protein YccA, indicating SecY level is controlled by FtsH and YccA. While the mutation of ftsH enhances SecY expression but diminishes bacterial stress resistance and virulence, which is similar to the phenotype caused by secY interference. Further works show that mutation of ftsH causes abnormal increase in secreted proteins and severely damaged cell membrane. We also find that secY overexpression leads to increased protein secretion and reduced survival in adversity, which is consistent with the result of secY interference. Taken together, we for the first time indicate that the homeostasis of SecY level is critical for normal physiological function of E. piscicida, which is conducive to understand the roles of SecY in bacterial stress resistance and pathogenicity.