Although both protein arginine methylation (PRMT) and jasmonate (JA) signaling are crucial for regulating plant development, the relationship between these processes in the control of spikelet development remains unclear. In this study, we used the CRISPR/Cas9 technology to generate two loss-of-function mutants that exhibit various abnormal spikelet structures. Interestingly, we found that OsPRMT6a can methylate arginine residues in JA signal repressors OsJAZ1 and OsJAZ7. We showed that arginine methylation of OsJAZ1 enhances the binding affinity of OsJAZ1 with the JA receptors OsCOI1a and OsCOI1b in the presence of JAs, thereby promoting the ubiquitination of OsJAZ1 by the SCF complex and degradation via the 26S proteasome. This process ultimately releases OsMYC2, a core transcriptional regulator in the JA signaling pathway, to activate or repress JA-responsive genes, thereby maintaining normal plant (spikelet) development. However, in the mutant, reduced arginine methylation of OsJAZ1 impaires the interaction between OsJAZ1 and OsCOI1a/OsCOI1b in the presence of JAs. As a result, OsJAZ1 proteins become more stable, repressing JA responses, thus causing the formation of abnormal spikelet structures. Moreover, we discovered that JA signaling reduces the mRNA level in an OsMYC2-dependent manner, thereby establishing a negative feedback loop to balance JA signaling. We further found that OsPRMT6a-mediated arginine methylation of OsJAZ1 likely serves as a switch to tune JA signaling to maintain normal spikelet development under harsh environmental conditions such as high temperatures. Collectively, our study establishes a direct molecular link between arginine methylation and JA signaling in rice.

中文翻译：

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OsPRMT6a 介导的 OsJAZ1 精氨酸甲基化调节水稻茉莉酸信号传导和小穗发育


尽管蛋白质精氨酸甲基化（PRMT）和茉莉酸（JA）信号对于调节植物发育至关重要，但这些过程在控制小穗发育中的关系仍不清楚。在本研究中，我们使用 CRISPR/Cas9 技术生成了两种表现出各种异常小穗结构的功能丧失突变体。有趣的是，我们发现OsPRMT6a可以甲基化JA信号抑制子OsJAZ1和OsJAZ7中的精氨酸残基。我们发现，在 JAs 存在的情况下，OsJAZ1 的精氨酸甲基化增强了 OsJAZ1 与 JA 受体 OsCOI1a 和 OsCOI1b 的结合亲和力，从而促进了 OsJAZ1 被 SCF 复合物泛素化并通过 26S 蛋白酶体降解。这个过程最终释放出JA信号通路中的核心转录调节因子OsMYC2，以激活或抑制JA响应基因，从而维持正常的植物（小穗）发育。然而，在突变体中，OsJAZ1 精氨酸甲基化的减少会损害 OsJAZ1 和 OsCOI1a/OsCOI1b 之间的相互作用（在 JAs 存在的情况下）。结果，OsJAZ1 蛋白变得更加稳定，抑制 JA 反应，从而导致异常小穗结构的形成。此外，我们发现JA信号以OsMYC2依赖性方式降低mRNA水平，从而建立负反馈环来平衡JA信号。我们进一步发现 OsPRMT6a 介导的 OsJAZ1 精氨酸甲基化可能作为调节 JA 信号传导的开关，以在高温等恶劣环境条件下维持正常的小穗发育。总的来说，我们的研究建立了水稻中精氨酸甲基化和 JA 信号传导之间的直接分子联系。