Axons Degenerate in the Absence of Mitochondria in C. elegans
Author(s)Rawson, Randi L.; Yam, Lung; Weimer, Robby M.; Bend, Eric G.; Horvitz, H. Robert; Clark, Scott G.; Jorgensen, Erik M.; Hartwieg, Erika A.; ... Show more Show less
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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 . 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.
DepartmentMassachusetts Institute of Technology. Department of Biology
Rawson, Randi L., Lung Yam, Robby M. Weimer, Eric G. Bend, Erika Hartwieg, H. Robert Horvitz, Scott G. Clark, and Erik M. Jorgensen. “Axons Degenerate in the Absence of Mitochondria in C. Elegans.” Current Biology 24, no. 7 (March 2014): 760–765. © 2014 Elsevier Ltd.
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