Shan Dongqian, Wang Chanyu, Zheng Xiaodong, Hu Zehui, Zhu Yunpeng, Zhao Yu, Jiang Awei, Zhang Haixia, Shi Kun, Bai Yixue, Yan Tianci, Wang Lin, Sun Yanzhao, Li Jianfang, Zhou Zhaoyang, Guo Yan, Kong Jin
College of Horticulture, China Agricultural University, Beijing 100193, China.
College of Biological Sciences, China Agricultural University, Beijing 100193, China.
Plant Physiol. 2021 Jun 11;186(2):1202-1219. doi: 10.1093/plphys/kiab108.
Glomerella leaf spot (GLS), a fungal disease caused by Colletotrichum fructicola, severely affects apple quality and yield, yet few resistance genes have been identified in apple (Malus domestica Borkh.). Here we found a transcription factor MdWRKY17 significantly induced by C. fructicola infection in the susceptible apple cultivar "Gala." MdWRKY17 overexpressing transgenic "Gala" plants exhibited increased susceptibility to C. fructicola, whereas MdWRKY17 RNA-interference plants showed opposite phenotypes, indicating MdWRKY17 acts as a plant susceptibility factor during C. fructicola infection. Furthermore, MdWRKY17 directly bound to the promoter of the salicylic acid (SA) degradation gene Downy Mildew Resistant 6 (MdDMR6) and promoted its expression, resulting in reduced resistance to C. fructicola. Additionally, Mitogen-activated protein kinase (MAPK) 3 (MdMPK3) directly interacted with and phosphorylated MdWRKY17. Importantly, predicted phosphorylation residues in MdWRKY17 by MAPK kinase 4 (MdMEK4)-MdMPK3 were critical for the activity of MdWRKY17 to regulate MdDMR6 expression. In the six susceptible germplasms, MdWRKY17 levels were significantly higher than the six tolerant germplasms after infection, which corresponded with lower SA content, confirming the critical role of MdWRKY17-mediated SA degradation in GLS tolerance. Our study reveals a rapid regulatory mechanism of MdWRKY17, which is essential for SA degradation and GLS susceptibility, paving the way to generate GLS resistant apple.
炭疽叶枯病（GLS）是由胶孢炭疽菌引起的一种真菌病害，严重影响苹果的品质和产量，但在苹果（Malus domestica Borkh.）中鉴定出的抗性基因很少。在这里，我们发现转录因子MdWRKY17在感病苹果品种“嘎啦”中受胶孢炭疽菌感染显著诱导。过表达MdWRKY17的转基因“嘎啦”植株对胶孢炭疽菌的敏感性增加，而MdWRKY17 RNA干扰植株表现出相反的表型，表明MdWRKY17在胶孢炭疽菌感染期间作为植物感病因子起作用。此外，MdWRKY17直接结合水杨酸（SA）降解基因抗霜霉病6（MdDMR6）的启动子并促进其表达，导致对胶孢炭疽菌的抗性降低。此外，丝裂原活化蛋白激酶（MAPK）3（MdMPK3）直接与MdWRKY17相互作用并使其磷酸化。重要的是，MAPK激酶4（MdMEK4）-MdMPK3预测的MdWRKY17磷酸化残基对于MdWRKY17调节MdDMR6表达的活性至关重要。在六种感病种质中，感染后MdWRKY17水平显著高于六种耐病种质，这与较低的SA含量相对应，证实了MdWRKY17介导的SA降解在炭疽叶枯病耐受性中的关键作用。我们的研究揭示了MdWRKY17的快速调控机制，这对于SA降解和炭疽叶枯病易感性至关重要，为培育抗炭疽叶枯病的苹果铺平了道路。
