文献类型：期刊文献

英文题名：Edwardsiella induces microtubule-severing in host epithelial cells

作者：Aggarwal, Priyanka[1];Wei, Lifan[2];Cao, Yuping[3];Liu, Qin[2,4,5];Guttman, Julian A.[1];Wang, Qiyao[2,4,5];Leung, Ka Yin[3]

机构：[1]Simon Fraser Univ, Fac Sci, Dept Biol Sci, 8888 Univ Dr, Burnaby, BC V5A 1S6, Canada;[2]East China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai, Peoples R China;[3]Guangdong Technion, Israel Inst Technol, 241 Xue Rd, Shantou 515063, Guangdong, Peoples R China;[4]Shanghai Engn Res Ctr Marine Cultured Anim Vaccin, Shanghai, Peoples R China;[5]Shanghai Collaborat Innovat Ctr Biomfg, Shanghai, Peoples R China

年份：2019

卷号：229

外文期刊名：MICROBIOLOGICAL RESEARCH

收录：;EI(收录号：20193907477054);WOS:【SCI-EXPANDED(收录号:WOS:000510806100009)】；

基金：JAG, QW, and KYL conceived and designed the study. PA, LW, and YC performed the experiments. QL, JAG, QW, and KYL provided strains or reagents. PA, JAG, and KYL drafted the paper. All authors contributed to and approved the manuscripts in its final format. This research was supported by the National Natural Science Foundation of China (grant number #31873048) and the National Science and Engineering Research Council of Canada (grant number #06385-2014) to Dr. Ka Yin Leung.

语种：英文

外文关键词：E. piscicida; Fish pathogen; Microtubule disassembly; Interaction with epithelial cells

摘要：Edwardsiella bacteria cause economic losses to a variety of commercially important fish globally. Human infections are rare and result in a gastroenteritis-like illness. Because these bacteria are evolutionarily related to other Enterobacteriaceae and the host cytoskeleton is a common target of enterics, we hypothesized that Edwardsiella may cause similar phenotypes. Here we use HeLa and Caco-2 infection models to show that microtubules are severed during the late infections. This microtubule alteration phenotype was not dependant on the type III or type VI secretion system (T3SS and T6SS) of the bacteria as Delta T3SS and Delta T6SS mutants of E. piscicida EIB202 and E. tarda ATCC15947 that lacks both also caused microtubule disassembly. Immunolocalization experiments showed the host katanin catalytic subunits A1 and A like 1 proteins at regions of microtubule severing, suggesting their involvement in the microtubule disassembly events. To identify bacterial components involved in this phenotype, we screened a 2,758 transposon library of E. piscicida EIB202 and found that 4 single mutations in the aipFHAGDC operon disrupted microtubule disassembly in HeLa cells. We then constructed three atp deletion mutants; they all could not disassemble host microtubules. This work provides the first clear evidence of host cytoskeletal alterations during Edwardsiella infections.