Mitochondrial MsrB2 serves as a switch and transducer for mitophagy

ABSTRACT: Mitophagy can selectively remove damaged toxic mitochondria, protecting a cell from apoptosis. The molecular spatial-temporal mechanisms governing autophagosomal selection of an ROS damaged mitochondria, particularly in a platelet (no genomic DNA for transcriptional regulation) remains unclear. We now report that the mitochondria matrix protein MsrB2 plays an important role in switching on mitophagy by reducing Parkin Methionine Oxidation (MetO), and transducing mitophagy through ubiquitination by Parkin and interacting with LC3. This biochemical signaling only occurs at damaged mitochondria where MsrB2 is released from the mitochondria matrix. MsrB2 platelet specific knockout, and in vivo peptide inhibition of the MsrB2/LC3 interaction leads to reduced mitophagy and increased platelet a

SUBMITTER: Dr. Seung Hee Lee 

PROVIDER: S-SCDT-EMM-2019-10409 | biostudies-other |

REPOSITORIES: biostudies-other