Chen Kun, Zhuang Yuhui, Chen Hua, Lei Taijie, Li Mengke, Wang Shanshan, Wang Lihui, Fu Huiwen, Lu Wenzhi, Bohra Abhishek, Lai Qiaoqiao, Xu Xiaolin, Garg Vanika, Barmukh Rutwik, Ji Biaojun, Zhang Chong, Pandey Manish K, Tang Ronghua, Varshney Rajeev K, Zhuang Weijian
Center for Legume Plant Genetics and Systems Biology, Oil Crops Research Institute, Fujian Agriculture and Forestry University, Fuzhou, 350002, China.
State Key Laboratory of Ecological Pest Control for Fujian and Taiwan Crops, College of Agriculture, Fujian Agriculture and Forestry University, Fuzhou, 350002, China.
Plant J. 2025 Jan;121(2):e17210. doi: 10.1111/tpj.17210.
Bacterial wilt caused by Ralstonia solanacearum is a devastating disease affecting a great many crops including peanut. The pathogen damages plants via secreting type Ш effector proteins (T3Es) into hosts for pathogenicity. Here, we characterized RipAU was among the most toxic effectors as ΔRipAU completely lost its pathogenicity to peanuts. A serine residue of RipAU is the critical site for cell death. The RipAU targeted a subtilisin-like protease (AhSBT1.7) in peanut and both protein moved into nucleus. Heterotic expression of AhSBT1.7 in transgenic tobacco and Arabidopsis thaliana significantly improved the resistance to R. solanacearum. The enhanced resistance was linked with the upregulating ERF1 defense marker genes and decreasing pectin methylesterase (PME) activity like PME2&4 in cell wall pathways. The RipAU played toxic effect by repressing R-gene, defense hormone signaling, and AhSBTs metabolic pathways but increasing PMEs expressions. Furthermore, we discovered AhSBT1.7 interacted with AhPME4 and was colocalized at nucleus. The AhPME speeded plants susceptibility to pathogen via mediated cell wall degradation, which inhibited by AhSBT1.7 but upregulated by RipAU. Collectively, RipAU impaired AhSBT1.7 defense for pathogenicity by using PME-mediated cell wall degradation. This study reveals the mechanism of RipAU pathogenicity and AhSBT1.7 resistance, highlighting peanut immunity to bacterial wilt for future improvement.
由青枯雷尔氏菌引起的青枯病是一种毁灭性病害，影响包括花生在内的许多作物。该病原菌通过向宿主分泌Ⅲ型效应蛋白（T3Es）来致病。在此，我们鉴定出RipAU是毒性最强的效应蛋白之一，因为缺失RipAU的菌株对花生完全丧失了致病性。RipAU的一个丝氨酸残基是细胞死亡的关键位点。RipAU靶向花生中的一种枯草杆菌蛋白酶样蛋白酶（AhSBT1.7），且两种蛋白都进入细胞核。AhSBT1.7在转基因烟草和拟南芥中的杂种优势表达显著提高了对青枯雷尔氏菌的抗性。增强的抗性与上调ERF1防御标记基因以及降低细胞壁途径中果胶甲酯酶（PME）如PME2和PME4的活性有关。RipAU通过抑制R基因、防御激素信号传导和AhSBTs代谢途径，但增加PMEs的表达来发挥毒性作用。此外，我们发现AhSBT1.7与AhPME4相互作用并共定位于细胞核。AhPME通过介导细胞壁降解加速植物对病原体的易感性，这一过程受到AhSBT1.7的抑制，但被RipAU上调。总体而言，RipAU通过利用PME介导的细胞壁降解来损害AhSBT1.7的致病性防御。本研究揭示了RipAU的致病机制和AhSBT1.7的抗性机制，突出了花生对青枯病的免疫力，以供未来改良。
