Brief Communication abstract


Nature Neuroscience 12, 387 - 389 (2009)
Published online: 15 March 2009 | Corrected online: 15 May 2009 | doi:10.1038/nn.2290

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

Bradley R Miller1, Craig Press2, Richard W Daniels1, Yo Sasaki2, Jeffrey Milbrandt2 & Aaron DiAntonio1

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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.

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  1. Department of Developmental Biology, Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, Missouri, USA.
  2. Department of Pathology, Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, Missouri, USA.

Correspondence to: Aaron DiAntonio1 e-mail: diantonio@wustl.edu

* In the version of this article initially published, the abbreviation DLK was omitted from the abstract. The second sentence of the abstract should be "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." The error has been corrected in the HTML and PDF versions of the article.

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