Liu Qianwei, Chen Xiao, Li Sujuan, Wang Qian, Liu Yusong, Zhang Zhijun, Yang Chao, Xu Shuo, Mao Ke, Ma Fengwang, Li Chao
State Key Laboratory for Crop Stress Resistance and High-Efficiency Production/Shaanxi Key Laboratory of Apple, College of Horticulture, Northwest A&F University, Yangling, Shaanxi, 712100, China.
Plant J. 2025 Jan;121(2):e17206. doi: 10.1111/tpj.17206. Epub 2024 Dec 11.
The plant cell wall is the first barrier against pathogen invasion. Fusarium solani is the primary pathogen responsible for apple replant disease. In this study, we identified an MYB protein, MdMYB54, which interacts with the positive regulator of F. solani resistance, MdERF114, and confers apple-increased tolerance against F. solani. The cellulose synthetase (CESA) gene MdCesA6 and pectin lyase-like (PLL) genes MdPLL8 and MdPLL12 were screened as three potential downstream target genes of MdMYB54 using DAP-seq. The results of electrophoretic mobility shift and yeast one-hybrid assays showed that MdMYB54 directly binds to the promoters of MdCesA6, MdPLL8, and MdPLL12 in vivo and in vitro. Dual-luciferase and β-glucuronidase assays showed that MdMYB54 activates the expression of these genes. The cellulose content and pectin lyase activity of MdMYB54-overexpressed roots were significantly higher than those of wild-type plants under F. solani treatment but were the opposite in MdMYB54-RNAi roots. The deposition of cellulose enhanced the physical barrier of the plant cell wall, whereas the activation of pectin lyase promoted the formation of oligogalacturonides and the production of reactive oxygen species. Overexpression of MdCesA6, MdPLL8, and MdPLL12 in the root system enhanced the tolerance of apple to F. solani. The direct interaction of MdERF114 with MdMYB54 enhanced MdMYB54-mediated cell wall defense response. These results suggest that modifying these candidate genes may provide a strategy for improving the resistance of apple to F. solani.
植物细胞壁是抵御病原体入侵的第一道屏障。茄腐镰刀菌是导致苹果再植病的主要病原体。在本研究中，我们鉴定出一种MYB蛋白MdMYB54，它与茄腐镰刀菌抗性的正向调节因子MdERF114相互作用，并赋予苹果对茄腐镰刀菌更强的耐受性。利用DAP-seq筛选出纤维素合成酶（CESA）基因MdCesA6以及果胶裂解酶样（PLL）基因MdPLL8和MdPLL12作为MdMYB54的三个潜在下游靶基因。电泳迁移率变动分析和酵母单杂交试验结果表明，MdMYB54在体内和体外均直接结合MdCesA6、MdPLL8和MdPLL12的启动子。双荧光素酶和β-葡萄糖醛酸酶试验表明，MdMYB54激活这些基因的表达。在茄腐镰刀菌处理下，MdMYB54过表达根系的纤维素含量和果胶裂解酶活性显著高于野生型植株，但在MdMYB54-RNAi根系中则相反。纤维素的沉积增强了植物细胞壁的物理屏障，而果胶裂解酶的激活促进了寡半乳糖醛酸的形成和活性氧的产生。在根系中过表达MdCesA6、MdPLL8和MdPLL12可增强苹果对茄腐镰刀菌的耐受性。MdERF114与MdMYB54的直接相互作用增强了MdMYB54介导的细胞壁防御反应。这些结果表明，修饰这些候选基因可能为提高苹果对茄腐镰刀菌的抗性提供一种策略。
