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Ubiquitination of ABCE1 by NOT4 in Response to Mitochondrial Damage Links Co-translational Quality Control to PINK1-Directed Mitophagy.

Cell Metab.. 2018; 
WuZhihao,WangYan,LimJunghyun,LiuBoxiang,LiYanping,VartakRasika,StankiewiczTrisha,MontgomeryStephen,LuBin
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Mutagenesis Services For making the ABCE1 K20R mutant, we chose 20 ABCE1 identified ubiquitination sites (K64, K116, K121, K128, K158, K165, K169, K178, K181, K191, K210, K250, K332, K343, K397, K412, K451, K579, K584, K590) from mUbiSiDa and modified them by changing AAG or AAA (K) to aga (R). All mutagenesis was done by GenScript Biotech Get A Quote

摘要

Translation of mRNAs is tightly regulated and constantly surveyed for errors. Aberrant translation can trigger co-translational protein and RNA quality control processes, impairments of which cause neurodegeneration by still poorly understood mechanism(s). Here we show that quality control of translation of mitochondrial outer membrane (MOM)-localized mRNA intersects with the turnover of damaged mitochondria, both orchestrated by the mitochondrial kinase PINK1. Mitochondrial damage causes stalled translation of complex-I 30 kDa subunit (C-I30) mRNA on MOM, triggering the recruitment of co-translational quality control factors Pelo, ABCE1, and NOT4 to the ribosome/mRNA-ribonucleoprotein complex. Damage... More

关键词

ABCE1,NOT4,PINK1,autophagy receptor recruitment,co-translational quality control,mitochondrial quality control,mitophagy,ribosome stalling,ribosome/mRNP remodeling,ubiquitina