Ya-Wen He, Calvin Boon, Lian Zhou, Lian-Hui Zhang*.
Institute of Molecular and Cell Biology, 61 Biopolis Drive, Singapore 138673
* Corresponding author: Dr. Lian-Hui ZHANG email@example.com,edu.sg
Published in Molecular Microbiology (2009) 71(6): 1464-1476
Xanthomonas campestris pv. campestris (Xcc) is known to regulate virulence through a quorum sensing (QS) mechanism. Detection of the QS signal DSF by sensor RpfC leads to activation of the response regulator RpfG, which influences virulence by degrading c-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 c-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 signaling 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.