The large size of neurons provides additional challenges for mitochondrial quality control, as the organelle is transported all over the axonal arbor and needs to function far away from the cell body and the bulk of the protein synthesis machinery. Local translation of mitochondrial proteins may alleviate some of this strain, and we have described mitochondrial hitchhiking as a novel method of mRNA transport. This neuron-specific mechanism ensures the local supply of freshly synthesized mitochondrial proteins to axonal mitochondria, allowing the repair or removal of potentially hazardous organelles.
We aim to discover the underlying mechanisms that regulate local translation of mitochondrial proteins and to analyze the adaption of this important organelle in response to neuronal activity in health and disease. A decline in mitochondrial health is a hallmark of many neurodegenerative disorders, but mitochondrial plasticity also emerges as a contributor to regular synaptic function. Understanding the molecular mechanisms that govern mitochondrial health and functions in neurons will further our knowledge on how this important organelle cross-talks with our neurons and ultimately affects our brain and behavior.