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Co‐regulation of Xanthomonas campestris virulence by quorum sensing and a novel two‐component regulatory system RavS/RavR
Author(s) -
He YaWen,
Boon Calvin,
Zhou Lian,
Zhang LianHui
Publication year - 2009
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2009.06617.x
Subject(s) - virulence , biology , regulator , quorum sensing , response regulator , xanthomonas campestris , mutant , two component regulatory system , operon , xanthomonas , genetics , phenotype , gene , regulation of gene expression , regulator of g protein signaling , microbiology and biotechnology , signal transduction , gtpase activating protein , g protein
Summary Xanthomonas campestris pv. campestris ( Xcc ) is known to regulate virulence through a quorum‐sensing mechanism. Detection of the quorum‐sensing signal DSF by sensor RpfC leads to activation of the response regulator RpfG, which influences virulence by degrading cyclic‐di‐GMP and by subsequent increasing expression of the global regulator Clp. In this study, we show that mutation of a response regulator RavR containing the GGDEF–EAL domains decreases Xcc virulence factor production . The functionality of RavR is dependent on its EAL domain‐associated cyclic‐di‐GMP phosphodiesterase activity. Deletion of a multidomain sensor gene ravS , which shares the same operon with ravR , results in similar phenotype changes as the ravR mutant. In addition, the sensor mutant phenotypes can be rescued by in trans expression of the response regulator, supporting the notion that RavS and RavR constitute a two‐component regulatory system. Significantly, mutation of either the PAS domain or key residues of RavS implicated in sensing low‐oxygen tension abrogates the sensor activity in virulence regulation. Moreover, similar to the DSF signalling system, RavS/RavR regulates virulence gene expression through the global regulator Clp. These results outline a co‐regulation mechanism that allows Xcc to integrate population density and environmental cues to modulate virulence factor production and adaptation.