A bacterial effector triggers dual-layer plant immunity through interaction with cell-surface and intracellular proteins.

Abstract

Plants deploy a two-layered immune system, comprising pattern-triggered immunity (PTI) and effector-triggered immunity (ETI), to defend against pathogens. Although PTI and ETI pathways converge on similar downstream responses, they are activated by distinct molecules at the cell surface and in the cytoplasm, respectively. Here, we report that the harpin-like effector RipW from Ralstonia solanacearum localizes to both the apoplastic and intracellular compartments, where it acts as a dual elicitor capable of activating PTI-like and ETI-like responses. We show that RipW triggers PTI-like responses through the receptor-like kinase RLK902 and its associated downstream signaling kinase BRASSINOSTEROID-SIGNALING KINASE1 (BSK1), while it physically interacts with the COP9 signalosome subunit 5 (CSN5), which contributes to the full activation of RipW-triggered ETI-like responses. Despite their roles in immune activation, knockdown of either RLK902 or CSN5 did not alter plant resistance against bacterial wilt caused by wild-type R. solanacearum because other type III effectors from the pathogen interfere with the two immune signaling pathways triggered by RipW. We further demonstrate that RLK902-mediated PTI-like responses are compromised by effectors RipAJ and RipG1, while CSN5-mediated ETI-like responses are suppressed by RipAF1 and RipN, respectively. Our findings reveal a unique pathogenic tactic, wherein a single effector triggers dual immune layers, and a corresponding virulence strategy, wherein the pathogen employs ancillary effectors to neutralize this elicited immunity.