Virulence factor regulator (Vfr) controls virulence‐associated phenotypes in Pseudomonas syringae pv. tabaci 6605 by a quorum sensing‐independent mechanism. (12th November 2012)

• Record Type: Journal Article
• Authors: Taguchi, Fumiko; Ichinose, Yuki
• Is Part Of: Molecular plant pathology. Volume 14:Number 3(2013:Apr.)
• Page Start: 279
• Page End: 292
• Publication Date: 2012-11-12
• Subjects: Plant diseases -- Molecular aspects -- Periodicals; Plant-pathogen relationships -- Molecular aspects -- Periodicals; 571.936
• DOI: 10.1111/mpp.12003
• Languages: English
• ISSNs: 1464-6722

Abstract

<abstract abstract-type="main"> <title>Summary</title> <p>Virulence factor regulator (Vfr) is a member of the cyclic 3′, 5′‐adenosine monophosphate (cAMP) receptor proteins that regulate the expression of many important virulence genes in <italic>Pseudomonas aeruginosa</italic>. The role of Vfr in pathogenicity has not been elucidated fully in phytopathogenic bacteria. To investigate the function of Vfr in <italic>Pseudomonas syringae</italic> pv. <italic>tabaci</italic> 6605, the <italic>vfr</italic> gene was disrupted. The virulence of the <italic>vfr</italic> mutant towards host tobacco plants was attenuated significantly, and the intracellular cAMP level was decreased. The <italic>vfr</italic> mutant reduced the expression of flagella‐, pili‐ and type III secretion system‐related genes and the defence response in nonhost <italic>Arabidopsis</italic> leaves. Furthermore, the expression levels of achromobactin‐related genes and the iron uptake ability were decreased, suggesting that Vfr regulates positively these virulence‐related genes. In contrast, the <italic>vfr</italic> mutant showed higher tolerance to antimicrobial compounds as a result of the enhanced expression of the resistance–nodulation–division family members, the <italic>mexA</italic>, <italic>mexB</italic> and <italic>oprM</italic> genes. We further demonstrated that the mutant strains of <italic>vfr</italic> and <italic>cyaA, </italic> an adenylate cyclase gene responsible for cAMP synthesis, showed a similar phenotype, suggesting that Vfr regulates virulence factors in a cAMP‐dependent manner. Because there was no significant difference in the production of acylhomoserine lactone (AHL) quorum sensing molecules in the wild‐type, <italic>vfr</italic> and <italic>cyaA</italic> mutant strains, Vfr might control important virulence factors by an AHL‐independent mechanism in an early stage of infection by this bacterium.</p> </abstract>