文摘
| Figures/TablesFigures/Tables | ReferencesReferences
Summary
Many neurodegenerative disorders are associated with mitochondrial defects []. Mitochondria can play an active role in degeneration by releasing reactive oxygen species and apoptotic factors []. 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 []. Here, we identify a C.聽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.聽elegans axons.
