Peri-mitochondrial actin filament inhibit Parkin assembly via disruption of ER-mitochondrial contact

ABSTRACT: Mitochondrial damage represents a dramatic change in cellular homeostasis, necessitating metabolic adaptation and clearance of the damaged organelle. One rapid response to mitochondrial damage is peri-mitochondrial actin polymerization within 2 mins, which we term ADA (Acute Damage-induced Actin). ADA is vital for a metabolic shift from oxidative phosphorylation to glycolysis upon mitochondrial dysfunction. In the current study we investigated the effect of ADA on Pink1/Parkin mediated mitochondrial quality control. We show that inhibition of proteins involved in the ADA pathway significantly accelerates Parkin recruitment onto depolarized mitochondria. Addressing the mechanism by which ADA resists Parkin recruitment onto depolarized mitochondria, we found that ADA disrupts ER-mitochondria

SUBMITTER: Tak Shun Fung 

PROVIDER: S-SCDT-10_1038-S44319-025-00561-Y | biostudies-other |

REPOSITORIES: biostudies-other