Abstract

The complex and elaborate architecture of a neuron poses a great challenge to the cellular machinery which localizes proteins and organelles, such as mitochondria, to necessary locations. Proper mitochondrial localization in neurons is particularly important as this organelle provides energy and metabolites essential to form and maintain functional neural connections. Consequently, maintenance of a healthy pool of mitochondria and removal of damaged organelles are essential for neuronal homeostasis. Long distance transport of the organelle itself as well as components necessary for maintaining mitochondria in distal compartments are important for a constant supply of healthy mitochondria at the right time and place. Accordingly, many neurodegenerative diseases have been associated with mitochondrial abnormalities. Here, we review our current understanding on transport-dependent mechanisms that regulate mitochondrial replenishment. We focus on axonal transport and import of mRNAs and proteins destined for mitochondria as well as mitochondrial fusion and fission to maintain mitochondrial homeostasis in distal compartments of the neuron.

Highlights

  • Neurons have one of the largest and most complex architectures of all cells in the human body

  • This study has found mitochondrial proteins are synthesized on the late endosomes which share close physical proximity to mitochondria (Cioni et al, 2019)

  • MRNAs can be transported with local translation occurring in distal neuronal compartments

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Summary

Introduction

Neurons have one of the largest and most complex architectures of all cells in the human body. Mutations in several motor proteins important for mitochondrial transport have been associated with neurodegenerative diseases. Instead of focusing on a well-covered topic, we will review recent developments in two mechanisms important for maintenance of this organelle in the neuron which require axonal transport: replenishment of mitochondrial proteins through active transport of proteins and their precursor mRNAs and mitochondrial dynamics.

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