Summary Plants employ nucleotide‐binding site‐leucine‐rich repeat (NBS‐LRR) proteins to monitor pathogen‐secreted proteins and initiate innate immune responses. This naturally raises the question of how pathogens subvert the NBS‐LRR protein‐mediated resistance. Here, we characterize a nucleus‐localized effector, Vne1, secreted by Colletotrichum gloeosporioides , the causal agent of Glomerella leaf spot of apple ( Malus × domestica ). We reveal that Vne1 interacts directly with the ‘PRGRP’ residues of MdAHL17, an apple AHL protein. Our findings indicate that MdAHL17 acts as a transcription factor (TF) governing the expression of MdCNL1 . We further show that MdCNL1 encodes a coiled‐coil‐NBS‐LRR protein that enhances apple resistance to C . gloeosporioides . Furthermore, we demonstrate that MdAHL17 binds directly to the promoter region of MdCNL1 through an AT‐rich element characterized by a ‘TATATATATT’ motif. Our study highlights that Vne1 interferes with the DNA‐binding affinity of MdAHL17, thereby perturbing MdCNL1‐mediated immunity. This elucidates a sophisticated mechanism through which fungal effectors strategically target the TF to subvert the resistance conferred by NBS‐LRR proteins during pathogen invasion.
Wang et al. (Mon,) studied this question.
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