Wallerian degeneration: an emerging axon death pathway linking injury and disease
Author:
Publisher
Springer Science and Business Media LLC
Subject
General Neuroscience
Link
http://www.nature.com/articles/nrn3680.pdf
Reference153 articles.
1. Samuel, M. A., Zhang, Y., Meister, M. & Sanes, J. R. Age-related alterations in neurons of the mouse retina. J. Neurosci. 31, 16033–16044 (2011).
2. Beirowski, B. et al. The progressive nature of Wallerian degeneration in wild-type and slow Wallerian degeneration (WldS) nerves. BMC Neurosci. 6, 6 (2005).
3. Mack, T. G. et al. Wallerian degeneration of injured axons and synapses is delayed by a Ube4b/Nmnat chimeric gene. Nature Neurosci. 4, 1199–1206 (2001). This study identifies the UBE4B–NMNAT1 fusion protein as WLDS, the causal factor delaying axon degeneration for up to 2 weeks after axon injury, by reproducing the phenotype in transgenic mice. It also reports that this protein is particularly abundant in neuronal nuclei.
4. Osterloh, J. M. et al. dSarm/Sarm1 is required for activation of an injury-induced axon death pathway. Science 337, 481–484 (2012). This study uses D. melanogaster genetics to identify a novel pro-axon death protein SARM1. Deletions of dSarm1 in D. melanogaster or its mouse orthologue remarkably delay injury-induced axon degeneration tenfold both in vivo and in primary neuronal culture, comparable to the effect of WLDS.
5. Babetto, E., Beirowski, B., Russler, E. V., Milbrandt, J. & Diantonio, A. The Phr1 ubiquitin ligase promotes injury-induced axon self-destruction. Cell Rep. 3, 1422–1429 (2013). This study shows that the mammalian ubiquitin ligase PHR1 is at least partly responsible for the turnover of NMNAT2. Its conditional deletion delays Wallerian degeneration both in vivo with an effect approaching that of WLDS, and to a lesser extent in primary neuronal cultures.
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