Journal
SCIENCE
Volume 337, Issue 6093, Pages 481-484Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1223899
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Funding
- U.S. Department of Defense [BC093796]
- National Institute for Neurological Diseases and Stroke (NINDS) [R01NS072248, U54NS065712, R01NS059991]
- Alzheimer's Research UK [ART/PG2009/2]
- Biotechnology and Biological Sciences Research Council Institute
- NIH [AI030165]
- Rockefeller University
- ALS Therapy Alliance
- NINDS ARRA [RC2-NS070-342]
- Angel Fund
- ALS Association
- P2ALS
- ALS
- Pierre L. de Bourgknecht ALS Research Foundation
- [NINDS5RO1-NS050557-05]
- Alzheimers Research UK [ART-PG2009-2] Funding Source: researchfish
- Biotechnology and Biological Sciences Research Council [BBS/E/B/0000C200, BBS/E/B/000C0417] Funding Source: researchfish
- BBSRC [BBS/E/B/000C0417] Funding Source: UKRI
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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 alpha/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.
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