SummaryGlomerella leaf spot (GLS), caused by the fungus Colletotrichum fructicola, is considered one of the most destructive diseases affecting apples. The VQ‐WRKY complex plays a crucial role in the response of plants to biotic stresses. However, our understanding of the defensive role of the VQ‐WRKY complex on woody plants, particularly apples, under biotic stress, remains limited. In this study, we elucidated the molecular mechanisms underlying the defensive role of the apple MdVQ37‐MdWRKY100 module in response to GLS infection. The overexpression of MdWRKY100 enhanced resistance to C. fructicola, whereas MdWRKY100 RNA interference in apple plants reduced resistance to C. fructicola by affecting salicylic acid (SA) content and the expression level of the CC‐NBS‐LRR resistance gene MdRPM1. DAP‐seq, Y1H, EMSA, and RT‐qPCR assays indicated that MdWRKY100 inhibited the expression of MdWRKY17, a positive regulatory factor gene of SA degradation, upregulated the expression of MdPAL1, a key enzyme gene of SA biosynthesis, and promoted MdRPM1 expression by directly binding to their promotors. Transient overexpression and silencing experiments showed that MdPAL1 and MdRPM1 positively regulated GLS resistance in apples. Furthermore, the overexpression of MdVQ37 increased the susceptibility to C. fructicola by reducing the SA content and expression level of MdRPM1. Additionally, MdVQ37 interacted with MdWRKY100, which repressed the transcriptional activity of MdWRKY100. In summary, these results revealed the molecular mechanism through which the apple MdVQ37‐MdWRKY100 module responds to GLS infection by regulating SA content and MdRPM1 expression, providing novel insights into the involvement of the VQ‐WRKY complex in plant pathogen defence responses.

中文翻译：

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MdVQ37-MdWRKY100 复合物调节水杨酸含量和 MdRPM1 表达，以调节苹果对肾小球叶斑病的抗性

摘要肾小球叶斑病 (GLS)，由真菌引起果炭疽菌，被认为是影响苹果最具破坏性的疾病之一。 VQ-WRKY 复合物在植物对生物胁迫的响应中发挥着至关重要的作用。然而，我们对 VQ-WRKY 复合物在生物胁迫下对木本植物（尤其是苹果）的防御作用的了解仍然有限。在这项研究中，我们阐明了苹果 MdVQ37-MdWRKY100 模块响应 GLS 感染的防御作用的分子机制。的过度表达MDWRKY100增强抵抗力C。果蝇属，而苹果植物中的 MdWRKY100 RNA 干扰降低了对C。果蝇属通过影响水杨酸（SA）含量和CC-NBS-LRR抗性基因的表达水平中速转速1。 DAP-seq、Y1H、EMSA 和 RT-qPCR 检测表明 MdWRKY100 抑制MdWRKY17，SA降解的正调控因子基因，上调表达中度PAL1，SA生物合成的关键酶基因，并促进中速转速1通过直接结合到它们的启动子来表达。瞬时过表达和沉默实验表明，MdPAL1 和 MdRPM1 正向调节苹果的 GLS 抗性。此外，过度表达MdVQ37增加了对以下疾病的敏感性C。果蝇属通过降低 SA 含量和表达水平中速转速1。此外，MdVQ37 与 MdWRKY100 相互作用，抑制 MdWRKY100 的转录活性。总之，这些结果揭示了苹果MdVQ37-MdWRKY100模块通过调节SA含量和响应GLS感染的分子机制。中速转速1表达，为 VQ-WRKY 复合物参与植物病原体防御反应提供了新的见解。