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|a Rawson, Randi L.
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|a Massachusetts Institute of Technology. Department of Biology
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|a Hartwieg, Erika A.
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|a Horvitz, H. Robert
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|a Yam, Lung
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|a Weimer, Robby M.
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|a Bend, Eric G.
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|a Clark, Scott G.
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|a Jorgensen, Erik M.
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|a Hartwieg, Erika A.
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|a Horvitz, Howard Robert
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|a Axons Degenerate in the Absence of Mitochondria in C. elegans
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|b Elsevier,
|c 2015-04-08T18:21:53Z.
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|z Get fulltext
|u http://hdl.handle.net/1721.1/96465
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|a 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.
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|a en_US
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|a Article
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|t Current Biology
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