Wallerian degeneration of injured axons and synapses is delayed by a Ube4b/Nmnat chimeric gene View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2001-12

AUTHORS

Till G.A. Mack, Michael Reiner, Bogdan Beirowski, Weiqian Mi, Monica Emanuelli, Diana Wagner, Derek Thomson, Tom Gillingwater, Felipe Court, Laura Conforti, F. Shama Fernando, Andrea Tarlton, Christian Andressen, Klaus Addicks, Giulio Magni, Richard R. Ribchester, V. Hugh Perry, Michael P. Coleman

ABSTRACT

Axons and their synapses distal to an injury undergo rapid Wallerian degeneration, but axons in the C57BL/WldS mouse are protected. The degenerative and protective mechanisms are unknown. We identified the protective gene, which encodes an N-terminal fragment of ubiquitination factor E4B (Ube4b) fused to nicotinamide mononucleotide adenylyltransferase (Nmnat), and showed that it confers a dose-dependent block of Wallerian degeneration. Transected distal axons survived for two weeks, and neuromuscular junctions were also protected. Surprisingly, the Wld protein was located predominantly in the nucleus, indicating an indirect protective mechanism. Nmnat enzyme activity, but not NAD+ content, was increased fourfold in WldS tissues. Thus, axon protection is likely to be mediated by altered ubiquitination or pyridine nucleotide metabolism. More... »

PAGES

1199

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nn770

DOI

http://dx.doi.org/10.1038/nn770

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1028133498

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/11770485


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