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

A DLK-dependent axon self-destruction program promotes Wallerian degeneration

A DLK And JNK Dependent Axon Self-Destruction Program Promotes Wallerian Degeneration

ii ACKNOWLEDGEMENTS iii

Motor axon excitability during Wallerian degeneration.

Axonal loss and degeneration are major factors in determining long-term outcome in patients with peripheral nerve disorders or injury. Following loss of axonal continuity, the isolated nerve stump distal to the lesion undergoes Wallerian degeneration in several phases. In the initial 'latent' phase, action potential propagation and structural integrity of the distal segment are maintained. The ...

Axon degeneration: Molecular mechanisms of a self-destruction pathway

Axon degeneration is a characteristic event in many neurodegenerative conditions including stroke, glaucoma, and motor neuropathies. However, the molecular pathways that regulate this process remain unclear. Axon loss in chronic neurodegenerative diseases share many morphological features with those in acute injuries, and expression of the Wallerian degeneration slow (WldS) transgene delays ner...

The Phr1 ubiquitin ligase promotes injury-induced axon self-destruction.

Axon degeneration is an evolutionarily conserved process that drives the loss of damaged axons and is an early event in many neurological disorders, so it is important to identify the molecular constituents of this poorly understood mechanism. Here, we demonstrate that the Phr1 E3 ubiquitin ligase is a central component of this axon degeneration program. Loss of Phr1 results in prolonged surviv...