SAMM50 是基础片段性线粒体自噬的受体，与 SQSTM1/p62 在 OXPHOS 诱导的线粒体自噬中协同作用。
SAMM50 is a receptor for basal piecemeal mitophagy and acts with SQSTM1/p62 in OXPHOS-induced mitophagy.
机构信息
Autophagy Research Group, Department of Medical Biology, University of Tromsø, the Arctic University of Norway, Tromsø, Norway.
Structural Biology Science Technology Platform, The Francis Crick Institute, London, UK.
出版信息
Autophagy. 2021 Sep;17(9):2656-2658. doi: 10.1080/15548627.2021.1953846. Epub 2021 Jul 18.
Mitophagy, the clearance of surplus or damaged mitochondria or mitochondrial parts by autophagy, is important for maintenance of cellular homeostasis. Whereas knowledge on programmed and stress-induced mitophagy is increasing, much less is known about mechanisms of basal mitophagy. Recently, we identified SAMM50 (SAMM50 sorting and assembly machinery component) as a receptor for piecemeal degradation of components of the sorting and assembly machinery (SAM) complex and mitochondrial contact site and cristae organizing system (MICOS) complexes. SAMM50 interacts directly with Atg8-family proteins through a canonical LIR motif and with SQSTM1/p62 to mediate basal piecemeal mitophagy. During a metabolic switch to oxidative phosphorylation (OXPHOS), SAMM50 cooperates with SQSTM1 to mediate efficient piecemeal mitophagy.
线粒体自噬是通过自噬清除多余或受损的线粒体或线粒体部分，对于维持细胞内稳态很重要。虽然程序性和应激诱导的线粒体自噬的知识在不断增加，但对于基础线粒体自噬的机制知之甚少。最近，我们发现 SAMM50（SAMM50 分选和装配机制成分）是分选和装配机制（SAM）复合物和线粒体接触位点和嵴组织系统（MICOS）复合物组件进行片段降解的受体。SAMM50 通过经典的 LIR 基序直接与 Atg8 家族蛋白相互作用，并与 SQSTM1/p62 相互作用，介导基础片段线粒体自噬。在代谢向氧化磷酸化（OXPHOS）的转变过程中，SAMM50 与 SQSTM1 合作，有效地进行片段线粒体自噬。
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