Li Jiahao, Yu Guolong, Wang Xinyuan, Guo Chaocheng, Wang Yudong, Wang Xu
Shanghai Collaborative Innovation Center of Agri-Seeds, Joint Center for Single Cell Biology, School of Agriculture and Biology, Shanghai Jiao Tong University, Shanghai 200240, China.
Shanghai Collaborative Innovation Center of Agri-Seeds, Joint Center for Single Cell Biology, School of Agriculture and Biology, Shanghai Jiao Tong University, Shanghai 200240, China.
Plant Commun. 2025 Jan 13;6(1):101133. doi: 10.1016/j.xplc.2024.101133. Epub 2024 Sep 14.
Proper mitochondrial function is crucial to plant growth and development. Inhibition of mitochondrial translation leads to mitochondrial proteotoxic stress, which triggers a protective transcriptional response that regulates nuclear gene expression, commonly referred to as the mitochondrial unfolded protein response (UPR). Although the UPR has been extensively studied in yeast and mammals, very little is known about the UPR in plants. Here, we show that mitochondrial translational stress inhibits plant growth and development by inducing jasmonic acid (JA) biosynthesis and signaling. The inhibitory effect of mitochondrial translational stress on plant growth was alleviated in the JA-signaling-defective mutants coi1-2, myc2, and myc234. Genetic analysis indicated that Arabidopsis mitochondrial ribosomal protein L1 (MRPL1), a key factor in the UPR, regulates plant growth in a CORONATINE-INSENSITIVE 1 (COI1)-dependent manner. Moreover, under mitochondrial translational stress, MYC2 shows direct binding to G boxes in the ETHYLENE RESPONSE FACTOR 109 (ERF109) promoter. The induction of ERF109 expression enhances hydrogen peroxide production, which acts as a feedback loop to inhibit root growth. In addition, mutation of MRPL1 increases JA accumulation, reduces plant growth, and enhances biotic stress resistance. Overall, our findings reveal that JA plays an important role in mediating retrograde signaling under mitochondrial translational stress to balance plant growth and defense.
正常的线粒体功能对植物的生长发育至关重要。线粒体翻译的抑制会导致线粒体蛋白毒性应激，从而引发一种保护性转录反应，该反应调节核基因表达，通常被称为线粒体未折叠蛋白反应（UPR）。尽管UPR在酵母和哺乳动物中已得到广泛研究，但在植物中对其了解甚少。在此，我们表明线粒体翻译应激通过诱导茉莉酸（JA）生物合成和信号传导来抑制植物生长发育。在JA信号缺陷突变体coi1 - 2、myc2和myc234中，线粒体翻译应激对植物生长的抑制作用得到缓解。遗传分析表明，拟南芥线粒体核糖体蛋白L1（MRPL1）作为UPR中的关键因子，以一种依赖于冠菌素不敏感1（COI1）的方式调节植物生长。此外，在 mitochondrial translational stress 下，MYC2直接与乙烯反应因子109（ERF109）启动子中的G盒结合。ERF109表达的诱导增强了过氧化氢的产生，过氧化氢作为反馈环抑制根的生长。此外，MRPL1的突变增加了JA的积累，降低了植物生长，并增强了生物胁迫抗性。总的来说，我们的研究结果表明，JA在介导线粒体翻译应激下的逆行信号传导以平衡植物生长和防御方面发挥着重要作用。 （注：原文中“mitochondrial translational stress”直译为“线粒体翻译应激”，可能表述不太准确，或许有更合适的专业术语表达，你可根据实际情况调整。）
