Author's School

Graduate School of Arts & Sciences

Author's Department/Program

Biology and Biomedical Sciences: Neurosciences

Language

English (en)

Date of Award

5-24-2011

Degree Type

Dissertation

Degree Name

Doctor of Philosophy (PhD)

Chair and Committee

Aaron DiAntonio

Abstract

Axon loss is a debilitating consequence of a wide range of neurological conditions. As axons degenerate, they go through a stereotyped sequence of morphological changes termed Wallerian degeneration. It has long been hypothesized that there is an active axonal breakdown program, conceptually similar to apoptosis, which underlies Wallerian degeneration. However, the molecular pathways that accomplish this program in neurons have remained elusive. We demonstrate that dual leucine kinase: DLK) promotes degeneration of severed axons in Drosophila and mice, and its target JNK promotes degeneration locally in axons as they commit to degenerate. This pathway also promotes degeneration after chemotherapy exposure, and thus may be a component of a general axon self-destruction program.

DOI

https://doi.org/10.7936/K79K4889

Comments

Permanent URL: http://dx.doi.org/10.7936/K79K4889

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