The Pseudomonas syringae type III effectors AvrRpm1 and AvrRpt2 promote virulence dependent on the F-box protein COI1.

KEY III effectors AvrRpm1 and AvrRpt2 promote bacterial growth dependent on a COI1-mediated pathway in the absence of the RPM1 and RPS2 resistance proteins. The type III effectors, AvrRpm1 and AvrRpt2, promote bacterial virulence by suppressing host defense responses. The defense suppressing activities of AvrRpm1 and AvrRpt2 are best studied in the absence of the resistance proteins RPM1 and RPS2, which induce defense responses to them. We tested whether the type III effectors could modulate a CORONATINE INSENSITIVE1 (COI1)-mediated hormone signaling pathway to promote virulence. COI1 has been demonstrated to contribute in the induction of chlorosis during Pseudomonas syringae infection. By comparing the activity of inducibly expressed AvrRpm1-HA or AvrRpt2-HA in rpm1rps2 and rpm1rps2coi1 backgrounds, we demonstrate that both effectors promote bacterial growth dependent on a COI1-mediated pathway and additively with the action of coronatine (COR) and that AvrRpt2-HA induces COI1-dependent chlorosis. Further, PATHOGENESIS RELATED1 (PR-1) expression resulting from inducible expression of AvrRpm1-HA or AvrRpt2-HA is elevated in coi1 plants consistent with the effectors activating JA-signaling to antagonize SA-signaling. In addition, we found that AvrRpm1-HA or AvrRpt2-HA requires COI1 to promote bacterial growth through suppression of both SA-dependent and SA-independent defense responses. Collectively, these results indicate that type III effectors AvrRpm1 and AvrRpt2 promote bacterial virulence by targeting a COI1-dependent signaling pathway.

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