Edwardsiella piscicida requires SecY homeostasis facilitated by FtsH and YccA for stress resistance and virulence
文献类型: 外文期刊
作者: Wu, Qingjuan 1 ; Tian, Aijun 2 ; Xu, Jiarui 1 ; Fang, Qingjian 2 ; Huang, Huiqin 2 ; Hu, Yonghua 1 ;
作者机构: 1.Chinese Acad Trop Agr Sci, Zhanjiang Expt Stn, Zhanjiang 524013, Peoples R China
2.Chinese Acad Trop Agr Sci, Inst Trop Biosci & Biotechnol, Key Lab Biol & Genet Resources Trop Crops, Haikou 571101, Peoples R China
3.Hainan Inst Trop Agr Resources, Key Lab Biol & Genet Resources Trop Crops Hainan P, Haikou 571101, Peoples R China
4.Pilot Natl Lab Marine Sci & Technol, Lab Marine Biol & Biotechnol, Qingdao 266071, Peoples R China
5.Hainan Univ, Sch Marine Biol & Aquaculture, Haikou 570228, Peoples R China
6.Hainan Univ, State Key Lab Marine Resource Utilizat South China, Haikou 570228, Peoples R China
7.Huazhong Agr Univ, Coll Fisheries, Dept Aquat Anim Med, Wuhan 430070, Peoples R China
8.Hainan Prov Key Lab Funct Components Res & Utiliza, Haikou 571101, Peoples R China
关键词: Edwardsiella piscicida; SecY; Stress tolerance; Pathogenicity; Protein secretion
期刊名称:AQUACULTURE ( 影响因子:4.5; 五年影响因子:4.6 )
ISSN: 0044-8486
年卷期: 2024 年 582 卷
页码:
收录情况: SCI
摘要: 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.
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