Laboratory of Mitochondrial Dynamics, Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamadaoka, Suita, Osaka 565-0871, Japan.
Laboratory of Mitochondrial Dynamics, Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamadaoka, Suita, Osaka 565-0871, Japan.
Biochim Biophys Acta Gen Subj. 2022 Nov;1866(11):130203. doi: 10.1016/j.bbagen.2022.130203. Epub 2022 Jul 13.
Autophagy-dependent selective degradation of excess or damaged mitochondria, termed mitophagy, is a tightly regulated process necessary for mitochondrial quality and quantity control. Mitochondria are highly dynamic and major sites for vital cellular processes such as ATP and iron‑sulfur cluster biogenesis. Due to their pivotal roles for immunity, apoptosis, and aging, the maintenance of mitochondrial function is of utmost importance for cellular homeostasis. In yeast, mitophagy is mediated by the receptor protein Atg32 that is localized to the outer mitochondrial membrane. Upon mitophagy induction, Atg32 expression is transcriptionally upregulated, which leads to its accumulation on the mitochondrial surface and to recruitment of the autophagic machinery via its direct interaction with Atg11 and Atg8. Importantly, post-translational modifications such as phosphorylation further fine-tune the mitophagic response. This review summarizes the current knowledge about mitophagy in yeast and its connection with mitochondrial dynamics and the ubiquitin-proteasome system.
自噬依赖性的过量或受损线粒体的选择性降解，称为线粒体自噬，是一个严格调控的过程，对于线粒体的质量和数量控制是必要的。线粒体是高度动态的，是细胞中许多重要过程的主要场所，如 ATP 和铁硫簇生物发生。由于它们在免疫、细胞凋亡和衰老中的关键作用，维持线粒体功能对于细胞内稳态至关重要。在酵母中，线粒体自噬是由定位于外线粒体膜的受体蛋白 Atg32 介导的。在诱导线粒体自噬后，Atg32 的表达转录上调，导致其在线粒体表面积累，并通过与 Atg11 和 Atg8 的直接相互作用招募自噬机制。重要的是，如磷酸化等翻译后修饰进一步微调了线粒体自噬反应。本文综述了酵母中线粒体自噬的最新知识，以及它与线粒体动力学和泛素-蛋白酶体系统的联系。
