A Dual-Receptor System Mediates <i>p</i> -Coumaric Acid Sensing/Degradation for Enhanced Bacterial Virulence

Plants deploy diverse secondary metabolites for chemical defense against pathogens, and in response, phytopathogens have evolved elaborate counterstrategies to subvert host immunity. In this study, we demonstrate that <i>Pseudomonas syringae</i> pv <i>actinidiae</i> strain M228 (<i>Psa</i>_M228)─the causal agent of kiwifruit bacterial canker (KBC)─employs a dual-functional system to sense and degrade host-derived <i>p</i>-coumaric acid (<i>p</i>-CA), thereby neutralizing the host's chemical defense. Specifically, the kiwifruit host plant produces <i>p</i>-CA, which binds to histidine kinase CasK of <i>Psa</i>_M228's two-component signaling system CasKR, inhibiting response regulator CasR phosphorylation. This reduces CasR binding to the promoter region of <i>fleQ</i>, downregulating <i>hrpL</i> expression─a master regulator of Type III secretion system (T3SS), ultimately attenuating virulence. For counter-defense, <i>Psa</i>_M228 utilizes the HcaR (hydroxycinnamic acid regulator) receptor and <i>hca</i> gene cluster (encoding <i>p</i>-CA-degrading enzymes) to catabolize <i>p</i>-CA. This adaptation helps <i>Psa</i>_M228 evade plant immunity and restore virulence, revealing a host-pathogen arms race.