<i>Phytophthora</i> effector exploits WY module truncation to manipulate Nt-acetylation-mediated AtMBP-1 turnover and suppress plant immunity.

Abstract

<i>Phytophthora</i> pathogens deliver a repertoire of WY(L) modular effectors to disarm plant immunity. Understanding how these conserved modules mediate the interactions between <i>Phytophthora</i> effectors and host targets to manipulate plant immunity is crucial. Here, we identified two WY(L) modular paralogous effectors, PcAvh337a and PcAvh337b, essential for <i>Phytophthora capsici</i> virulence. Transposon insertion induced truncation of WY(L) module, enabling PcAvh337b to target <i>Arabidopsis</i> 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 <i>P. capsici</i> 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.