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Citation
Osterloh, J.M., Yang, J., Rooney, T.M., Fox, A.N., Adalbert, R., Powell, E.H., Sheehan, A.E., Avery, M.A., Hackett, R., Logan, M.A., MacDonald, J.M., Ziegenfuss, J.S., Milde, S., Hou, Y.J., Nathan, C., Ding, A., Brown, R.H., Conforti, L., Coleman, M., Tessier-Lavigne, M., Züchner, S., Freeman, M.R. (2012). dSarm/Sarm1 is required for activation of an injury-induced axon death pathway.  Science 337(6093): 481--484.
FlyBase ID
FBrf0219055
Publication Type
Research paper
Abstract

Axonal and synaptic degeneration is a hallmark of peripheral neuropathy, brain injury, and neurodegenerative disease. Axonal degeneration has been proposed to be mediated by an active autodestruction program, akin to apoptotic cell death; however, loss-of-function mutations capable of potently blocking axon self-destruction have not been described. Here, we show that loss of the Drosophila Toll receptor adaptor dSarm (sterile α/Armadillo/Toll-Interleukin receptor homology domain protein) cell-autonomously suppresses Wallerian degeneration for weeks after axotomy. Severed mouse Sarm1 null axons exhibit remarkable long-term survival both in vivo and in vitro, indicating that Sarm1 prodegenerative signaling is conserved in mammals. Our results provide direct evidence that axons actively promote their own destruction after injury and identify dSarm/Sarm1 as a member of an ancient axon death signaling pathway.

PubMed ID
PubMed Central ID
PMC5225956 (PMC) (EuropePMC)
Related Publication(s)
Note

Neuroscience. dSarm-ing axon degeneration.
Yu and Luo, 2012, Science 337(6093): 418--419 [FBrf0219076]

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    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Science
    Title
    Science
    Publication Year
    1895-
    ISBN/ISSN
    0036-8075
    Data From Reference
    Aberrations (10)
    Alleles (8)
    Genes (4)
    Natural transposons (1)
    Experimental Tools (2)
    Transgenic Constructs (5)