Edwardsiella piscicida, as an important pathogen of fish, has caused huge losses in aquaculture. The virulence in E. piscicida has been increasingly concerned, but few studies have focused on the relationship between virulence and protein secretion homeostasis. FtsH, as a member of the AAA protease family, has important cellular functions, such as controlling the quality of membrane proteins. In this study, FtsH was demonstrated to be essential in maintaining protein secretion homeostasis, and its deletion could result in the secretion of massive cytoplasmic proteins by non-classical secretion pathway. Furthermore it was showed that FtsH is vital for E. piscicida to proliferate within host cells, and E. piscicida mutant ΔftsH will be obviously attenuated. After zebrafish was infected with the mutant ΔftsH, the lethality rate for zebrafish and the bacterial colonization in its organs were greatly reduced. These results suggested that FtsH, as a regulatory factor, closely linked protein secretory homeostasis with bacterial virulence, which provided clues for further exploring the involvement of protein secretion homeostasis in bacterial virulence.

Edwardsiella piscicida作为鱼类的重要病原体，给水产养殖造成了巨大损失。E. piscicida的毒力越来越受到关注，但很少有研究关注毒力与蛋白质分泌稳态之间的关系。FtsH 作为 AAA 蛋白酶家族的一员，具有重要的细胞功能，例如控制膜蛋白的质量。在这项研究中，FtsH 被证明在维持蛋白质分泌稳态中是必不可少的，它的缺失可能导致大量细胞质蛋白通过非经典分泌途径分泌。此外，还表明 FtsH 对于E. piscicida在宿主细胞内增殖至关重要，而E. piscicida突变体 Δ ftsH会明显减弱。斑马鱼感染突变体Δ ftsH 后，斑马鱼的致死率和细菌在其器官中的定植率大大降低。这些结果表明FtsH作为调节因子，将蛋白质分泌稳态与细菌毒力密切相关，为进一步探索蛋白质分泌稳态在细菌毒力中的参与提供了线索。