An overview of the molecular mechanisms of mitophagy in yeast
An overview of the molecular mechanisms of mitophagy in yeast
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DOI：
10.1016/j.bbagen.2022.130203
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发表时间：
2022-11-01
影响因子：
3
通讯作者：
Okamoto，Koji
中科院分区：
文献类型：
--
作者：
Schuster，Ramona;Okamoto，Koji
过量或受损线粒体的自噬依赖性选择性降解（称为线粒体自噬）是线粒体质量和数量控制所必需的严格调控过程。线粒体是高度动态的重要细胞过程（例如 ATP 和铁硫簇生物合成）的主要场所。由于线粒体在免疫、细胞凋亡和衰老方面发挥着关键作用，因此维持线粒体功能对于细胞稳态至关重要。在酵母中，线粒体自噬是由位于线粒体外膜的受体蛋白 Atg32 介导的。线粒体自噬诱导后，Atg32 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，磷酸化等翻译后修饰进一步微调线粒体自噬反应。这篇综述总结了目前关于酵母线粒体自噬及其与线粒体动力学和泛素蛋白酶体系统的联系的知识。
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.