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Organism dual RNA‐seq reveals the importance of BarA/UvrY in Vibrio parahaemolyticus virulence
Author(s) -
Zhang Wenwen,
Xie Ruiqiang,
Zhang Xiaohua Douglas,
Lee Leo Tsz On,
Zhang Hongjie,
Yang Menghua,
Peng Bo,
Zheng Jun
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.201902630r
Subject(s) - vibrio parahaemolyticus , virulence , biology , pathogen , organism , microbiology and biotechnology , transcriptome , caenorhabditis elegans , host (biology) , rna interference , model organism , host–pathogen interaction , gene , innate immune system , rna , immune system , genetics , bacteria , gene expression
Elucidation of host‐pathogen interaction is essential for developing effective strategies to combat bacterial infection. Dual RNA‐Seq using cultured cells or tissues/organs as the host of pathogen has emerged as a novel strategy to understand the responses concurrently from both pathogen and host at cellular level. However, bacterial infection mostly causes systematic responses from the host at organism level where the interplay is urgently to be understood but inevitably being neglected by the current practice. Here, we developed an approach that simultaneously monitor the genome‐wide infection‐linked transcriptional alterations in both pathogenic Vibrio parahaemolyticus and the infection host nematode Caenorhabditis elegans . Besides the dynamic alterations in transcriptomes of both C. elegans and V. parahaemolyticus during infection, we identify a two‐component system, BarA/UvrY, that is important for virulence in host. BarA/UvrY not only controls the virulence factors in V. parahaemolyticus including Type III and Type VI secretion systems, but also attenuates innate immune responses in C. elegans , including repression on the MAP kinase‐mediated cascades. Thus, our study exemplifies the use of dual RNA‐Seq at organism level to uncover previously unrecognized interplay between host and pathogen.