Mitochondrial function is controlled by two separate genomes. This feature makes mitochondria prone to proteotoxic stress when a stoichiometric imbalance occurs in the protein complexes that perform oxidative phosphorylation, which consist of both nuclear- and mitochondrial-encoded proteins. Such a proteotoxic stress is known to induce the mitochondrial unfolded protein response (UPR^mt) in animals. It is unknown whether UPR^mt occurs in plants. Here, we induced a mitonuclear protein imbalance in Arabidopsis through chemical or genetic interference. Mitochondrial proteotoxic stress activated a plant-specific UPR^mt and impaired plant growth and development. The plant UPR^mt pathway is triggered by a transient oxidative burst, activating MAPK and hormonal (involving ethylene and auxin) signaling, which are all geared to repair proteostasis. This also establishes phytohormones as bona fide plant mitokines. Our data ascertain that mitochondrial protein quality control pathways, such as the UPR^mt, are conserved in plants and that hormone signaling is an essential mediator that regulates mitochondrial proteostasis.

线粒体功能由两个独立的基因组控制。当执行氧化磷酸化的蛋白质复合物发生化学计量失衡时，此特征使线粒体易于发生蛋白毒性应激，该蛋白质复合物由核和线粒体编码的蛋白质组成。已知这种蛋白毒性应激在动物中诱导线粒体未折叠的蛋白应答（UPR ^mt）。尚不清楚植物中是否存在UPR ^mt。在这里，我们通过化学或遗传干扰诱导了拟南芥中的微核蛋白失衡。线粒体蛋白毒性胁迫激活了植物特有的UPR ^mt，并损害了植物的生长发育。该厂UPR^吨瞬时氧化爆发，激活MAPK和激素（涉及乙烯和生长素）信号传导均触发该途径，这些信号都可以修复蛋白稳态。这也将植物激素确立为真正的植物mitokines。我们的数据确定了线粒体蛋白质质量控​​制途径（如UPR ^mt）在植物中是保守的，激素信号传导是调节线粒体蛋白稳态的重要介质。