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Demonstrates how Pseudomonas syringae modulates virulence through p-coumaric acid degradation in plants, suggesting an evolutionary arms race.
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 Pseudomonas syringae pv actinidiae strain M228 (Psa_M228)─the causal agent of kiwifruit bacterial canker (KBC)─employs a dual-functional system to sense and degrade host-derived p-coumaric acid (p-CA), thereby neutralizing the host's chemical defense. Specifically, the kiwifruit host plant produces p-CA, which binds to histidine kinase CasK of Psa_M228's two-component signaling system CasKR, inhibiting response regulator CasR phosphorylation. This reduces CasR binding to the promoter region of fleQ, downregulating hrpL expression─a master regulator of Type III secretion system (T3SS), ultimately attenuating virulence. For counter-defense, Psa_M228 utilizes the HcaR (hydroxycinnamic acid regulator) receptor and hca gene cluster (encoding p-CA-degrading enzymes) to catabolize p-CA. This adaptation helps Psa_M228 evade plant immunity and restore virulence, revealing a host-pathogen arms race.
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Zhang et al. (2026) studied this question.
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