Yang Ruirui, Su Chenglin, Xue Zhiyuan, Wei Hongbo, Wang Zhengjie, Zhu Jiaxuan, Meng Jun, Luan Yushi
MOE Key Laboratory of Bio-Intelligent Manufacturing, School of Bioengineering, Dalian University of Technology, Dalian, 116024, China.
School of Computer Science and Technology, Dalian University of Technology, Dalian, 116024, China.
Plant J. 2025 Mar;121(6):e70098. doi: 10.1111/tpj.70098.
Late blight, caused by Phytophthora infestans (P. infestans), seriously compromises tomato growth and yield. PAMP-induced peptides (PIPs) are secreted peptides that act as endogenous elicitors, triggering plant immune responses. Our previous research indicated that the exogenous application of PIP1 from Solanum pimpinelifolium L3708, named SpPIP1, enhances tomato resistance to P. infestans. However, little is known about the roles of additional family members in tomato resistance to P. infestans. In addition, there remains a significant gap in understanding the receptors of SpPIPs and the transcription factors (TFs) that regulate SpPIPs signaling in tomato defense, and the combination of SpPIPs signaling and TFs in defending against pathogens is rarely studied. This study demonstrates that the exogenous application of SpPIP-LIKE1 (SpPIPL1) also strengthens tomato resistance by affecting the phenylpropanoid biosynthesis pathway. Both SpPIP1 and SpPIPL1 trigger plant defense responses in a manner dependent on RLK7L. Tomato plants overexpressing the precursors of SpPIP1 and SpPIPL1 (SpprePIP1 and SpprePIPL1) exhibited enhanced expression of pathogenesis-related genes, elevated HO and ABA levels, and increased lignin accumulation. Notably, SpWRKY65 was identified as a transcriptional activator of SpprePIP1 and SpprePIPL1. Disease resistance assays and gene expression analyses revealed that overexpression of SpWRKY65 (OEWRKY65) confers tomato resistance to P. infestans, while wrky65 knockout led to the opposite effect. Intriguingly, transgenic tomato studies showed that either spraying OEWRKY65 with SpPIPs or co-overexpressing SpprePIP1 and SpWRKY65 further augmented tomato resistance, underscoring the potential of gene stacking in enhancing disease resistance. In summary, this study offers new perspectives on controlling late blight and developing tomato varieties with improved resistance. The results emphasize the potential of exogenous SpPIPs application as an eco-friendly strategy for crop protection, laying a theoretical foundation for advancing crop breeding.
由致病疫霉（Phytophthora infestans）引起的晚疫病严重影响番茄的生长和产量。病原体相关分子模式诱导的肽（PAMP-induced peptides，PIPs）是作为内源性激发子起作用的分泌肽，可触发植物免疫反应。我们之前的研究表明，来自醋栗番茄L3708的PIP1（命名为SpPIP1）的外源施用可增强番茄对致病疫霉的抗性。然而，关于该家族其他成员在番茄对致病疫霉抗性中的作用知之甚少。此外，在理解SpPIPs的受体以及在番茄防御中调节SpPIPs信号传导的转录因子（TFs）方面仍存在重大差距，并且很少研究SpPIPs信号传导与TFs在抵御病原体中的组合。本研究表明，外源施用类SpPIP1（SpPIP-LIKE1，SpPIPL1）也通过影响苯丙烷类生物合成途径增强番茄抗性。SpPIP1和SpPIPL1均以依赖于RLK7L的方式触发植物防御反应。过表达SpPIP1和SpPIPL1前体（SpprePIP1和SpprePIPL1）的番茄植株表现出病程相关基因的表达增强、H₂O₂和脱落酸（ABA）水平升高以及木质素积累增加。值得注意的是，SpWRKY65被鉴定为SpprePIP1和SpprePIPL1的转录激活因子。抗病性测定和基因表达分析表明，过表达SpWRKY65（OEWRKY65）赋予番茄对致病疫霉的抗性，而wrky65敲除则产生相反的效果。有趣的是，转基因番茄研究表明，用SpPIPs喷洒OEWRKY65或共过表达SpprePIP1和SpWRKY65进一步增强了番茄抗性，强调了基因叠加在增强抗病性方面的潜力。总之，本研究为控制晚疫病和培育抗性增强的番茄品种提供了新的视角。结果强调了外源施用SpPIPs作为一种生态友好型作物保护策略的潜力，为推进作物育种奠定了理论基础。
