• Journal of Life Science
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• v.21 no.2
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• pp.227-234
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• 2011

The hrp gene cluster in the plant pathogen Pseudomonas syringae is a key determinant of pathogenicity. Recent studies have demonstrated that specific host cell induction of the Ralstonia solanacearum hrp gene cluster is controlled by the PrhA (plant regulator of hrp) receptor. To characterize the role that P. syringae PrhA plays in the virulence of plant cells, a prhA homolog was isolated from P. syringae pv. tabaci and a $\Delta$prhA mutant was constructed by allelic exchange. The $\Delta$prhA mutant had reduced virulence in the host plant, and co-culture of P. syringae pv. tabaci and plant cell suspensions induced a much higher level of hrpA gene transcription than culture in hrp-inducing minimal medium. These results indicate that PrhA of P. syringae is a putative pathogen-plant cell contact sensor, therefore, we used a hrpA-gfp reporter fusion to monitor the in situ expression of PrhA. The results of this study demonstrated that PrhA induces hrp gene expression in P. syringae pv. tabaci in the presence of plant cells.

• Proceedings of the Korean Society of Life Science Conference
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• 2008.10a
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• pp.72.2-72.2
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• 2008

• Journal of Life Science
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• v.25 no.2
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• pp.136-150
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• 2015

Pseudomonas syringae pathovar tabaci is a plant pathogenic bacterium that causes wildfire disease in tobacco plants. In P. syringae pv. tabaci, PsyI, a LuxI-type protein, acts as an AHL synthase, while primary and secondary sequence analysis of PsyR has revealed that it is a homolog of the LuxR-type transcriptional regulator that responds to AHL molecules. In this study, using phenotypic and genetic analyses in P. syringae pv. tabaci, we show the effect of PsyR protein as a quorum-sensing (QS) transcriptional regulator. Regulatory effects of PsyR on swarming motility and production of siderophores, tabtoxin, and N-acyl homoserine lactones were examined via phenotypic assays, and confirmed by quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR). Further qRT-PCR showed that PsyR regulates expression of these virulence genes in response to environmental signals. However, an upstream region of the gene was not bound with purified MBP-PsyR protein; rather, PsyR was only able to shift the upstream region of psyI. These results suggested that PsyR may be indirectly controlled via intermediate-regulatory systems and that auto-regulation by PsyR does not occur.