The roles of a mitochondrial protein Miga in autophagy

被引:3
|
作者
Xu, Lingna [1 ,2 ,3 ]
Wang, Liquan [1 ]
Tong, Chao [1 ,2 ,3 ]
机构
[1] Zhejiang Univ, Sch Med, Affiliated Hosp 2, Life Sci Inst,Dept Obstet, Hangzhou 310009, Peoples R China
[2] Zhejiang Univ, Life Sci Inst, MOE Key Lab Biosyst Homeostasis & Protect, Hangzhou, Peoples R China
[3] Zhejiang Univ, Life Sci Inst, Innovat Ctr Cell Signaling Network, Hangzhou, Peoples R China
基金
中国国家自然科学基金;
关键词
Autophagy; drosophila; endoplasmic reticulum-mitochondrial contacts; mitochondrion; phosphatidylinositol-3; kinase;
D O I
10.1080/15548627.2022.2153569
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Miga is an evolutionarily conserved protein that localizes to the outer membrane of mitochondria and mediates endoplasmic reticulum (ER)-mitochondrial contacts through interaction with VAP proteins in the ER. We recently reported that Miga is required for autophagosome-lysosome fusion during macroautophagy/autophagy. Miga binds to Atg14 and Uvrag, two alternative subunits of the class III phosphatidylinositol 3-kinase (PtdIns3K) complex. Miga regulates phosphatidylinositol-3-phosphate (PtdIns3P) levels through its interaction with Uvrag and its ER-mitochondrial contact site (ERMCS) tethering activity. Miga stabilizes Atg14, which maintains steady levels of the SNARE protein, Syx17. We propose that Miga establishes a direct link between mitochondria and autophagy to maintain cellular homeostasis.
引用
收藏
页码:2151 / 2152
页数:2
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