A dual leucine kinase-dependent axon self-destruction program promotes Wallerian degeneration.

ABSTRACT: Axon degeneration underlies many common neurological disorders, but the signaling pathways that orchestrate axon degeneration are unknown. We found that dual leucine kinase (DLK) [corrected to add (DLK) abbreviation] promoted degeneration of severed axons in Drosophila and mice, and that its target, c-Jun N-terminal kinase, promoted degeneration locally in axons as they committed to degenerate. This pathway also promoted degeneration after chemotherapy exposure and may be a component of a general axon self-destruction program.

SUBMITTER: Miller BR 

PROVIDER: S-EPMC2696160 | biostudies-literature | 2009 Apr

REPOSITORIES: biostudies-literature