Schizophrenia-associated dysbindin modulates axonal mitochondrial movement in cooperation with p150^glued.

ABSTRACT: Mitochondrial movement in neurons is finely regulated to meet the local demand for energy and calcium buffering. Elaborate transport machinery including motor complexes is required to deliver and localize mitochondria to appropriate positions. Defects in mitochondrial transport are associated with various neurological disorders without a detailed mechanistic information. In this study, we present evidence that dystrobrevin-binding protein 1 (dysbindin), a schizophrenia-associated factor, plays a critical role in axonal mitochondrial movement. We observed that mitochondrial movement was impaired in dysbindin knockout mouse neurons. Reduced mitochondrial motility caused by dysbindin deficiency decreased the density of mitochondria in the distal part of axons. Moreover, the transport and dist

SUBMITTER: Suh BK 

PROVIDER: S-EPMC7814725 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature