Figure 12.

Working model of how XopS promotes Xcv virulence. A, Upon infection of pepper plants with an Xcv strain lacking XopS, WRKY40 ubiquitination results in its degradation by the proteasome and leads to the de-repression of its target genes. This enables the induction of SA-dependent gene expression, such as CaPR1, and at the same time represses JA-dependent responses through increased expression of negative regulators, including CaJAZ8. As a result, stomata close in response to MAMP perception and the plant mounts apoplastic defense responses. B, In contrast, WT Xcv delivers XopS into the host cell, which prevents degradation of WRKY40 through physical interaction. Stabilized WRKY40 attenuates the induction of SA-dependent immunity and also mediates decreased expression of CaJAZ8. The latter results in an activation of JA-responses further antagonizing SA-mediated defense, including interference with stomatal closure to facilitate bacterial tissue entry.