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Curr Biol. 2014 Mar 31;24(7):760-5. doi: 10.1016/j.cub.2014.02.025. Epub 2014 Mar 13.

Axons degenerate in the absence of mitochondria in C. elegans.

Author information

1
Department of Biology and Howard Hughes Medical Institute, University of Utah, Salt Lake City, UT 84112-0840, USA.
2
Molecular Neurobiology Program, Department of Pharmacology, Skirball Institute, NYU School of Medicine, New York, NY 10016, USA.
3
Howard Hughes Medical Institute and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
4
Department of Biology and Howard Hughes Medical Institute, University of Utah, Salt Lake City, UT 84112-0840, USA. Electronic address: jorgensen@biology.utah.edu.

Abstract

Many neurodegenerative disorders are associated with mitochondrial defects [1-3]. Mitochondria can play an active role in degeneration by releasing reactive oxygen species and apoptotic factors [4-7]. Alternatively, mitochondria can protect axons from stress and insults, for example by buffering calcium [8]. Recent studies manipulating mitochondria lend support to both of these models [9-13]. Here, we identify a C. elegans mutant, ric-7, in which mitochondria are unable to exit the neuron cell bodies, similar to the kinesin-1/unc-116 mutant. When axons lacking mitochondria are cut with a laser, they rapidly degenerate. Some neurons even spontaneously degenerate in ric-7 mutants. Degeneration can be suppressed by forcing mitochondria into the axons of the mutants. The protective effect of mitochondria is also observed in the wild-type: a majority of axon fragments containing a mitochondrion survive axotomy, whereas those lacking mitochondria degenerate. Thus, mitochondria are not required for axon degeneration and serve a protective role in C. elegans axons.

PMID:
24631238
PMCID:
PMC4018749
DOI:
10.1016/j.cub.2014.02.025
[Indexed for MEDLINE]
Free PMC Article

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