title: Axons degenerate in the absence of mitochondria in C. elegans.
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.
authors.affiliation: Department of Biology and Howard Hughes Medical Institute, University of Utah, Salt Lake City, UT 84112-0840, USA.
authors.forename: Randi L
authors.initials: RL
authors.lastname: Rawson
authors.affiliation: Molecular Neurobiology Program, Department of Pharmacology, Skirball Institute, NYU School of Medicine, New York, NY 10016, USA.
authors.forename: Lung
authors.initials: L
authors.lastname: Yam
authors.affiliation: Department of Biology and Howard Hughes Medical Institute, University of Utah, Salt Lake City, UT 84112-0840, USA.
authors.forename: Robby M
authors.initials: RM
authors.lastname: Weimer
authors.affiliation: Department of Biology and Howard Hughes Medical Institute, University of Utah, Salt Lake City, UT 84112-0840, USA.
authors.forename: Eric G
authors.initials: EG
authors.lastname: Bend
authors.affiliation: Howard Hughes Medical Institute and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
authors.forename: Erika
authors.initials: E
authors.lastname: Hartwieg
authors.affiliation: Howard Hughes Medical Institute and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
authors.forename: H Robert
authors.initials: HR
authors.lastname: Horvitz
authors.affiliation: Molecular Neurobiology Program, Department of Pharmacology, Skirball Institute, NYU School of Medicine, New York, NY 10016, USA.
authors.forename: Scott G
authors.initials: SG
authors.lastname: Clark
authors.affiliation: Department of Biology and Howard Hughes Medical Institute, University of Utah, Salt Lake City, UT 84112-0840, USA. Electronic address: jorgensen@biology.utah.edu.
authors.forename: Erik M
authors.initials: EM
authors.lastname: Jorgensen
mesh_terms: D000818:Animals; D001369:Axons / Q000502:physiology / Q000648:ultrastructure*; D019771:Axotomy; D017173:Caenorhabditis elegans / Q000166:cytology* / Q000502:physiology / Q000648:ultrastructure; D029742:Caenorhabditis elegans Proteins / Q000235:genetics; D002118:Calcium / Q000378:metabolism; D008928:Mitochondria / Q000502:physiology*; D009154:Mutation; D009410:Nerve Degeneration; D009419:Nerve Tissue Proteins / Q000235:genetics; D019636:Neurodegenerative Diseases; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D029742:Caenorhabditis elegans Proteins; D009419:Nerve Tissue Proteins; D017382:Reactive Oxygen Species; C572928:Ric-7 protein, C elegans; D002118:Calcium