The ZmWAKL–ZmWIK–ZmBLK1–ZmRBOH4 module provides quantitative resistance to gray leaf spot in maize

作者：Tao Zhong, Mang Zhu, Qianqian Zhang, Yan Zhang, Suining Deng, Chenyu Guo, Ling Xu, Tingting Liu, Yancong Li, Yaqi Bi, Xingming Fan, Peter Balint‐Kurti, Mingliang Xu · 发表于：Nature Genetics · 年份：2024 · DOI：10.1038/s41588-023-01644-z · 被引用次数：62 · 研究领域：Nematode management and characterization studies、Plant Disease Resistance and Genetics、Plant-Microbe Interactions and Immunity

Abstract Gray leaf spot (GLS), caused by the fungal pathogens Cercospora zeae-maydis and Cercospora zeina , is a major foliar disease of maize worldwide ( Zea mays L.). Here we demonstrate that ZmWAKL encoding cell-wall-associated receptor kinase-like protein is the causative gene at the major quantitative disease resistance locus against GLS. The ZmWAKL Y protein, encoded by the resistance allele, can self-associate and interact with a leucine-rich repeat immune-related kinase ZmWIK on the plasma membrane. The ZmWAKL Y /ZmWIK receptor complex interacts with and phosphorylates the receptor-like cytoplasmic kinase (RLCK) ZmBLK1, which in turn phosphorylates its downstream NADPH oxidase ZmRBOH4. Upon pathogen infection, ZmWAKL Y phosphorylation activity is transiently increased, initiating immune signaling from ZmWAKL Y , ZmWIK, ZmBLK1 to ZmRBOH4, ultimately triggering a reactive oxygen species burst. Our study thus uncovers the role of the maize ZmWAKL–ZmWIK–ZmBLK1–ZmRBOH4 receptor/signaling/executor module in perceiving the pathogen invasion, transducing immune signals, activating defense responses and conferring increased resistance to GLS.