Phytophthora effector exploits WY module truncation to manipulate Nt-acetylation–mediated AtMBP-1 turnover and suppress plant immunity

Phytophthora pathogens deliver a repertoire of WY(L) modular effectors to disarm plant immunity. Understanding how these conserved modules mediate the interactions between Phytophthora effectors and host targets to manipulate plant immunity is crucial. Here, we identified two WY(L) modular paralogous effectors, PcAvh337a and PcAvh337b, essential for Phytophthora capsici virulence. Transposon insertion induced truncation of WY(L) module, enabling PcAvh337b to target Arabidopsis cMyc binding protein 1 (AtMBP-1). While the existence of AtMBP-1 has been debated, this study demonstrates that alternative transcription initiation and translation can generate AtMBP-1, further revealing that AtMBP-1 compromises plant immune responses as a susceptibility factor. AtMBP-1 homeostasis is antagonistically regulated by N-terminal acetyltransferases A and C (NatA and NatC). By modulating AtMBP-1-Nat complexes, PcAvh337b enhances NatA-mediated acetylation of AtMBP-1 to protect AtMBP-1 from ubiquitin-dependent degradation, thereby promoting P. capsici infection. These findings reveal a pathogenic mechanism through which an effector regulates AtMBP-1-Nat modules to suppress plant defense responses, highlighting virulence mechanisms diversification driven by effector dynamics.