Mitochondrial Complex I and ROS control neuromuscular function through opposing pre- and postsynaptic mechanisms.

ABSTRACT: Neurons require high amounts energy, and mitochondria help to fulfill this requirement. Dysfunctional mitochondria trigger problems in various neuronal tasks. Using the Drosophila neuromuscular junction (NMJ) as a model synapse, we previously reported that Mitochondrial Complex I (MCI) subunits were required for maintaining NMJ function and growth. Here we report tissue-specific adaptations at the NMJ when MCI is depleted. In Drosophila motor neurons, MCI depletion causes profound cytological defects and increased mitochondrial reactive oxygen species (ROS). But instead of diminishing synapse function, neuronal ROS triggers a homeostatic signaling process that maintains normal NMJ excitation. We identify molecules mediating this compensatory response. MCI depletion in muscles

SUBMITTER: Mallik B 

PROVIDER: S-EPMC11722341 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature