Proposed model of the mode of inhibition of stomatal closure by Xcc. The DSF (diamonds), which mediates cell-to-cell communication, interacts with the cell surface receptor RpfC, which in turn triggers signaling that leads to transcription of genes required for the synthesis of the stomatal inhibitory compound (triangles). This molecule diffuses to the extracellular space and gets contact with stomatal guard cells, where it blocks stomatal closure induced by ABA or PAMPs by interfering with some signaling component within a putative signaling pathway branch including H₂O₂ and MPK3. MPK3 is absolutely required for bacterial or PAMP-induced promotion of closure pathway, as shown by the failure of MPK3 antisense plants to close stomata in response to these stimuli. For ABA, instead, other pathways, including ABA-induced cytosolic pH increase, would compensate for the absence of MPK3. The failure of the stomatal inhibitor to interfere with promotion of closure by ABA in MPK3 antisense plants could be explained by compensatory adjustments within the guard-cell-signaling network, indicated by thick arrows, that would make up for the absence of MPK3. WT, Wild type; LRR, Leu-rich repeat receptor.