Edwardsiella induces microtubule-severing in host epithelial cells

TY - JOUR

T1 - Edwardsiella induces microtubule-severing in host epithelial cells

AU - Aggarwal, Priyanka

AU - Wei, Lifan

AU - Cao, Yuping

AU - Liu, Qin

AU - Guttman, Julian A.

AU - Wang, Qiyao

AU - Leung, Ka Yin

N1 - Publisher Copyright: © 2019 The Authors

PY - 2019/12

Y1 - 2019/12

N2 - 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 ΔT3SS and ΔT6SS 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 atpFHAGDC 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.

AB - 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 ΔT3SS and ΔT6SS 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 atpFHAGDC 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.

KW - E. piscicida

KW - Fish pathogen

KW - Interaction with epithelial cells

KW - Microtubule disassembly

UR - http://www.scopus.com/inward/record.url?scp=85072609174&partnerID=8YFLogxK

U2 - 10.1016/j.micres.2019.126325

DO - 10.1016/j.micres.2019.126325

M3 - 文章

C2 - 31563838

AN - SCOPUS:85072609174

SN - 0944-5013

VL - 229

JO - Microbiological Research

JF - Microbiological Research

M1 - 126325

ER -