Endogenous salicylic acid (SA) regulates leaf senescence, but the underlying mechanism remains largely unexplored. The exogenous application of SA to living plants is not efficient for inducing leaf senescence. By taking advantage of probenazole (PBZ)‐induced biosynthesis of endogenous SA, we previously established a chemical inducible leaf senescence system that depends on SA biosynthesis and its core signaling receptor NPR1 in Arabidopsis thaliana. Here, using this system, we identified WRKY46 and WRKY6 as key components of the transcriptional machinery downstream of NPR1 signaling. Upon PBZ treatment, the wrky46 mutant exhibited significantly delayed leaf senescence. We demonstrate that NPR1 is essential for PBZ/SA‐induced WRKY46 activation, whereas WRKY46 in turn enhances NPR1 expression. WRKY46 interacts with NPR1 in the nucleus, binding to the W‐box of the WRKY6 promoter to induce its expression in response to SA signaling. Dysfunction of WRKY6 abolished PBZ‐induced leaf senescence, while overexpression of WRKY6 was sufficient to accelerate leaf senescence even under normal growth conditions, suggesting that WRKY6 may serve as an integration node of multiple leaf senescence signaling pathways. Taken together, these findings reveal that the NPR1‐WRKY46‐WRKY6 signaling cascade plays a critical role in PBZ/SA‐mediated leaf senescence in Arabidopsis.

中文翻译：

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NPR1-WRKY46-WRKY6信号级联介导拟南芥中丙苯唑/水杨酸引起的叶片衰老

内源性水杨酸 (SA) 调节叶片衰老，但其潜在机制在很大程度上仍未得到探索。SA 对活植物的外源应用对诱导叶片衰老无效。通过利用丙苯唑 (PBZ) 诱导的内源性 SA 生物合成，我们之前在拟南芥中建立了依赖于 SA 生物合成及其核心信号受体 NPR1 的化学诱导叶片衰老系统。在这里，使用该系统，我们将 WRKY46 和 WRKY6 确定为 NPR1 信号下游转录机制的关键组成部分。PBZ 处理后，wrky46突变体表现出显着延迟的叶片衰老。我们证明 NPR1 对于 PBZ/SA 诱导的WRKY46是必不可少的激活，而 WRKY46 反过来增强NPR1表达。WRKY46 与细胞核中的 NPR1 相互作用，与WRKY6启动子的 W-box 结合以响应 SA 信号诱导其表达。WRKY6 的功能障碍消除了 PBZ 诱导的叶片衰老，而WRKY6 的过表达即使在正常生长条件下也足以加速叶片衰老，表明 WRKY6 可能作为多个叶片衰老信号通路的整合节点。总之，这些发现表明 NPR1-WRKY46-WRKY6 信号级联在拟南芥中 PBZ/SA 介导的叶片衰老中起关键作用。