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A dual leucine kinase–dependent axon self-destruction program promotes Wallerian degeneration
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A dual leucine kinase–dependent axon self-destruction program promotes Wallerian degeneration
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Journal Article
A dual leucine kinase–dependent axon self-destruction program promotes Wallerian degeneration
2009
Overview
Axon degeneration is an active process. Miller and colleagues show in fly and mouse models that axon degeneration requires the kinase DLK and its downstream target JNK to proceed.
Axon degeneration underlies many common neurological disorders, but the signaling pathways that orchestrate axon degeneration are unknown. We found that dual leucine kinase (DLK) 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.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ Animals
/ Animals, Genetically Modified
/ Axons
/ Biomedical and Life Sciences
/ Enzyme Inhibitors - pharmacology
/ Green Fluorescent Proteins - genetics
/ JNK Mitogen-Activated Protein Kinases - genetics
/ JNK Mitogen-Activated Protein Kinases - metabolism
/ MAP Kinase Kinase Kinases - metabolism
/ Mice
/ Nerve Tissue Proteins - genetics
/ Olfactory Receptor Neurons - pathology
