Neurons are post-mitotic cells that must function throughout the life of an organism. The high energetic requirements and Ca2+ spikes of synaptic transmission place a burden on neuronal mitochondria. The removal of older mitochondria and the replenishment of the functional mitochondrial pool in axons with freshly synthesized components are therefore important parts of neuronal maintenance. Although the mechanism of mitochondrial protein import and dynamics is studied in great detail, the length of neurons poses additional challenges to those processes. In this mini-review, I briefly cover the basics of mitochondrial biogenesis and proceed to explain the interdependence of mitochondrial transport and mitochondrial health. I then extrapolate recent findings in yeast and mammalian cultured cells to neurons, making a case for axonal translation as a contributor to mitochondrial biogenesis in neurons.
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Cover Image
Cover Image
The Holliday junction. The structure of the Holliday junction is highly variable, being adaptable to its biological function in recombination and to applications in biomolecular engineering. This image shows the how the junction extends from simple schematics to crystal structures as DNA only and in protein complexes. In addition, the junction has been exploited as an element in the design of 2-D and 3-D lattices in crystal engineering and more complex images and shapes through DNA origami. In this issue of Biochemical Society Transactions, P. Shing Ho reviews some interesting recent research on the Holliday junction; for details see pages 1149–1158.
Mitochondrial health maintenance in axons
Angelika B. Harbauer; Mitochondrial health maintenance in axons. Biochem Soc Trans 15 October 2017; 45 (5): 1045–1052. doi: https://doi.org/10.1042/BST20170023
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