OPTN-ATG9 interaction accelerates autophagic degradation of ubiquitin-labeled mitochondria

(Tokyo Metropolitan Institute of Medical Science) Damaged mitochondria are selectively eliminated via autophagy (called mitophagy). Parkin and PINK1, proteins mutated in hereditary Parkinson's disease, amplify ubiquitin signals on damaged mitochondria with the subsequent activation of autophagic machinery. Researchers in the Ubiquitin Project of Tokyo Metropolitan Institute of Medical Science (TMIMS) discovered that the critical autophagy adaptor OPTN (optineurin) interacts with ATG9A, and this ...