Orf1B controls secretion of T3SS proteins and contributes to Edwardsiella piscicida adhesion to epithelial cells

Abstract Edwardsiella piscicida is a Gram-negative enteric pathogen that causes hemorrhagic septicemia in fish. The type III secretion system (T3SS) is one of its two most important virulence islands. T3SS protein EseJ inhibits E. piscicida adhesion to epithelioma papillosum cyprini (EPC) cells by n...

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Main Authors: Long Kun Wang, Shan Shan Sun, Shu Ya Zhang, Pin Nie, Hai Xia Xie
Format: Article
Language:English
Published: BMC 2022-06-01
Series:Veterinary Research
Subjects:
Online Access:https://doi.org/10.1186/s13567-022-01057-6
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author Long Kun Wang
Shan Shan Sun
Shu Ya Zhang
Pin Nie
Hai Xia Xie
author_facet Long Kun Wang
Shan Shan Sun
Shu Ya Zhang
Pin Nie
Hai Xia Xie
author_sort Long Kun Wang
collection DOAJ
description Abstract Edwardsiella piscicida is a Gram-negative enteric pathogen that causes hemorrhagic septicemia in fish. The type III secretion system (T3SS) is one of its two most important virulence islands. T3SS protein EseJ inhibits E. piscicida adhesion to epithelioma papillosum cyprini (EPC) cells by negatively regulating type 1 fimbria. Type 1 fimbria helps E. piscicida to adhere to fish epithelial cells. In this study, we characterized a functional unknown protein (Orf1B) encoded within the T3SS gene cluster of E. piscicida. This protein consists of 122 amino acids, sharing structural similarity with YscO in Vibrio parahaemolyticus. Orf1B controls secretion of T3SS translocon and effectors in E. piscicida. By immunoprecipitation, Orf1B was shown to interact with T3SS ATPase EsaN. This interaction may contribute to the assembly of the ATPase complex, which energizes the secretion of T3SS proteins. Moreover, disruption of Orf1B dramatically decreased E. piscicida adhesion to EPC cells due to the increased steady-state protein level of EseJ within E. piscicida. Taken together, this study partially unraveled the mechanisms through which Orf1B promotes secretion of T3SS proteins and contributes to E. piscicida adhesion. This study helps to improve our understanding on molecular mechanism of E. piscicida pathogenesis.
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spelling doaj.art-c792c13d3066472c8f49158668ea67ed2022-12-22T00:23:51ZengBMCVeterinary Research1297-97162022-06-0153111110.1186/s13567-022-01057-6Orf1B controls secretion of T3SS proteins and contributes to Edwardsiella piscicida adhesion to epithelial cellsLong Kun Wang0Shan Shan Sun1Shu Ya Zhang2Pin Nie3Hai Xia Xie4Dalian Ocean UniversityState Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of SciencesState Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of SciencesState Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of SciencesState Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of SciencesAbstract Edwardsiella piscicida is a Gram-negative enteric pathogen that causes hemorrhagic septicemia in fish. The type III secretion system (T3SS) is one of its two most important virulence islands. T3SS protein EseJ inhibits E. piscicida adhesion to epithelioma papillosum cyprini (EPC) cells by negatively regulating type 1 fimbria. Type 1 fimbria helps E. piscicida to adhere to fish epithelial cells. In this study, we characterized a functional unknown protein (Orf1B) encoded within the T3SS gene cluster of E. piscicida. This protein consists of 122 amino acids, sharing structural similarity with YscO in Vibrio parahaemolyticus. Orf1B controls secretion of T3SS translocon and effectors in E. piscicida. By immunoprecipitation, Orf1B was shown to interact with T3SS ATPase EsaN. This interaction may contribute to the assembly of the ATPase complex, which energizes the secretion of T3SS proteins. Moreover, disruption of Orf1B dramatically decreased E. piscicida adhesion to EPC cells due to the increased steady-state protein level of EseJ within E. piscicida. Taken together, this study partially unraveled the mechanisms through which Orf1B promotes secretion of T3SS proteins and contributes to E. piscicida adhesion. This study helps to improve our understanding on molecular mechanism of E. piscicida pathogenesis.https://doi.org/10.1186/s13567-022-01057-6T3SSOrf1BadhesionT3SS protein secretionEdwardsiella piscicida
spellingShingle Long Kun Wang
Shan Shan Sun
Shu Ya Zhang
Pin Nie
Hai Xia Xie
Orf1B controls secretion of T3SS proteins and contributes to Edwardsiella piscicida adhesion to epithelial cells
Veterinary Research
T3SS
Orf1B
adhesion
T3SS protein secretion
Edwardsiella piscicida
title Orf1B controls secretion of T3SS proteins and contributes to Edwardsiella piscicida adhesion to epithelial cells
title_full Orf1B controls secretion of T3SS proteins and contributes to Edwardsiella piscicida adhesion to epithelial cells
title_fullStr Orf1B controls secretion of T3SS proteins and contributes to Edwardsiella piscicida adhesion to epithelial cells
title_full_unstemmed Orf1B controls secretion of T3SS proteins and contributes to Edwardsiella piscicida adhesion to epithelial cells
title_short Orf1B controls secretion of T3SS proteins and contributes to Edwardsiella piscicida adhesion to epithelial cells
title_sort orf1b controls secretion of t3ss proteins and contributes to edwardsiella piscicida adhesion to epithelial cells
topic T3SS
Orf1B
adhesion
T3SS protein secretion
Edwardsiella piscicida
url https://doi.org/10.1186/s13567-022-01057-6
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