粒体自噬
自噬
生物
细胞生物学
生物发生
调节器
自噬体
ULK1
磷酸化
遗传学
基因
蛋白激酶A
细胞凋亡
安普克
作者
François Le Guerroué,Eric Bunker,William M. Rosencrans,Jack Nguyen,Mohammed A. Basar,Achim Werner,Tsui‐Fen Chou,Chunxin Wang,Richard J. Youle
出处
期刊:Molecular Cell
[Elsevier]
日期:2023-03-01
卷期号:83 (6): 927-941.e8
被引量:12
标识
DOI:10.1016/j.molcel.2023.02.023
摘要
Mitophagy is a form of selective autophagy that disposes of superfluous and potentially damage-inducing organelles in a tightly controlled manner. While the machinery involved in mitophagy induction is well known, the regulation of the components is less clear. Here, we demonstrate that TNIP1 knockout in HeLa cells accelerates mitophagy rates and that ectopic TNIP1 negatively regulates the rate of mitophagy. These functions of TNIP1 depend on an evolutionarily conserved LIR motif as well as an AHD3 domain, which are required for binding to the LC3/GABARAP family of proteins and the autophagy receptor TAX1BP1, respectively. We further show that phosphorylation appears to regulate its association with the ULK1 complex member FIP200, allowing TNIP1 to compete with autophagy receptors, which provides a molecular rationale for its inhibitory function during mitophagy. Taken together, our findings describe TNIP1 as a negative regulator of mitophagy that acts at the early steps of autophagosome biogenesis.
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