Axons Degenerate in the Absence of Mitochondria in C. elegans

• Main Authors: Rawson, Randi L (Author), Yam, Lung (Author), Weimer, Robby M (Author), Bend, Eric G (Author), Clark, Scott G. (Author), Jorgensen, Erik M. (Author), Hartwieg, Erika A. (Contributor), Horvitz, Howard Robert (Author)
• Other Authors: Massachusetts Institute of Technology. Department of Biology (Contributor), Horvitz, H. Robert (Contributor)
• Format: Article
• Language: English
• Published: Elsevier, 2015-04-08T18:21:53Z.
• Subjects: Article
• Online Access: Get fulltext

 Many neurodegenerative disorders are associated with mitochondrial defects [1, 2 and 3]. Mitochondria can play an active role in degeneration by releasing reactive oxygen species and apoptotic factors [4, 5, 6 and 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, 10, 11, 12 and 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.