中文版 | English
Title

The phospholipase effector Tle1Vc promotes Vibrio cholerae virulence by killing competitors and impacting gene expression

Author
Corresponding AuthorFu,Yang
Publication Years
2023
DOI
Source Title
ISSN
1949-0976
EISSN
1949-0984
Volume15Issue:1
Abstract
Vibrio cholerae utilizes the Type VI secretion system (T6SS) to gain an advantage in interbacterial competition by delivering anti-prokaryotic effectors in a contact-dependent manner. However, the impact of T6SS and its secreted effectors on physiological behavior remains poorly understood. In this study, we present Tle1, a phospholipase effector in atypical pathogenic V. cholerae E1 that is secreted by T6SS via its interaction with VgrG1. Tle1 contains a DUF2235 domain and belongs to the Tle1 (type VI lipase effector) family. Bacterial toxicity assays, lipase activity assays and site-directed mutagenesis revealed that Tle1 possessed phospholipase A activity and phospholipase A activity, and that Tle1-induced toxicity required a serine residue (S356) and two aspartic acid residues (D417 and D496). Cells intoxication with Tle1 lead to membrane depolarization and alter membrane permeability. Tli1, a cognate immunity protein, directly interacts with Tle1 to neutralize its toxicity. Moreover, Tle1 can kill multiple microorganisms by T6SS and promote in vivo fitness of V. cholerae through mediating antibacterial activity. Tle1 induces bacterial motility by increasing the expression of flagellar-related genes independently of functional T6SS and the tit-for-tat (TFT) response, where Pseudomonas aeruginosa uses its T6SS-H1 cluster to counterattack other offensive attackers. Our study also demonstrated that the physical puncture of E1 T6SS can induce a moderate TFT response, which is essential to the Tle1-mediated strong TFT response, maximizing effector functions. Overall, our study characterized the antibacterial mechanism of phospholipase effector Tle1 and its multiple physiological significance.
Keywords
URL[Source Record]
Indexed By
Language
English
SUSTech Authorship
First ; Corresponding
Funding Project
National Natural Science Foundation of China[32270061]
WOS Research Area
Gastroenterology & Hepatology ; Microbiology
WOS Subject
Gastroenterology & Hepatology ; Microbiology
WOS Accession No
WOS:001038523700001
Publisher
Scopus EID
2-s2.0-85166151620
Data Source
Scopus
Citation statistics
Cited Times [WOS]:0
Document TypeJournal Article
Identifierhttp://kc.sustech.edu.cn/handle/2SGJ60CL/560198
DepartmentSchool of Medicine
Affiliation
1.School of Medicine,Southern University of Science and Technology,Shenzhen,China
2.College of Life Sciences,Nanjing Agricultural University,Nanjing,China
First Author AffilicationSchool of Medicine
Corresponding Author AffilicationSchool of Medicine
First Author's First AffilicationSchool of Medicine
Recommended Citation
GB/T 7714
Liu,Ming,Wang,Heng,Liu,Ying,et al. The phospholipase effector Tle1Vc promotes Vibrio cholerae virulence by killing competitors and impacting gene expression[J]. Gut Microbes,2023,15(1).
APA
Liu,Ming.,Wang,Heng.,Liu,Ying.,Tian,Miao.,Wang,Zhao.,...&Fu,Yang.(2023).The phospholipase effector Tle1Vc promotes Vibrio cholerae virulence by killing competitors and impacting gene expression.Gut Microbes,15(1).
MLA
Liu,Ming,et al."The phospholipase effector Tle1Vc promotes Vibrio cholerae virulence by killing competitors and impacting gene expression".Gut Microbes 15.1(2023).
Files in This Item:
There are no files associated with this item.
Related Services
Fulltext link
Recommend this item
Bookmark
Usage statistics
Export to Endnote
Export to Excel
Export to Csv
Altmetrics Score
Google Scholar
Similar articles in Google Scholar
[Liu,Ming]'s Articles
[Wang,Heng]'s Articles
[Liu,Ying]'s Articles
Baidu Scholar
Similar articles in Baidu Scholar
[Liu,Ming]'s Articles
[Wang,Heng]'s Articles
[Liu,Ying]'s Articles
Bing Scholar
Similar articles in Bing Scholar
[Liu,Ming]'s Articles
[Wang,Heng]'s Articles
[Liu,Ying]'s Articles
Terms of Use
No data!
Social Bookmark/Share
No comment.

Items in the repository are protected by copyright, with all rights reserved, unless otherwise indicated.