ArticlePLoS genetics2022
Divergent signaling requirements of dSARM in injury-induced degeneration and developmental glial phagocytosis.
Article in PLoS genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- Light- and temperature-sensitive seizures are regulated by spatially distinct cortex glial populations in the central nervous system.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Raw defines a TIR-fold cADPR hydrolase cooperating with dSarm in development and axon degeneration.Cell communication and signaling : CCS · 2026Article
- Glia Preserve Their Own Functions While Compensating for Neighboring Glial Cell Dysfunction.Glia · 2025Article
- Article
- Glial Regulation of Circuit Wiring, Firing, and Expiring in theCold Spring Harbor perspectives in biology · 2024Review
- Glia control experience-dependent plasticity in an olfactory critical period.bioRxiv : the preprint server for biology · 2024Article
- SARM1-Dependent Axon Degeneration: Nucleotide Signaling, Neurodegenerative Disorders, Toxicity, and Therapeutic Opportunities.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024Review
- Article
- Drosophila glia take shape to sculpt the nervous system.Current opinion in neurobiology · 2023Review
- A nerve-wracking buzz: lessons fromFrontiers in aging neuroscience · 2023Review
- Opposing roles of Fos, Raw, and SARM1 in the regulation of axonal degeneration and synaptic structure.Frontiers in cellular neuroscience · 2023Article
- Early Draper-mediated glial refinement of neuropil architecture and synapse number in the Drosophila antennal lobe.Frontiers in cellular neuroscience · 2023Article
- Distinct developmental and degenerative functions of SARM1 require NAD+ hydrolase activity.PLoS genetics · 2022Article
- Multifaceted roles of SARM1 in axon degeneration and signaling.Frontiers in cellular neuroscience · 2022Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Elucidating signal transduction mechanisms of innate immune pathways is essential to defining how they elicit distinct cellular responses. Toll-like receptors (TLR) signal through their cytoplasmic TIR domains which bind other TIR domain-containing adaptors. dSARM/SARM1 is one such TIR domain adaptor best known for its role as the central axon degeneration trigger after injury. In degeneration, SARM1's domains have been assigned unique functions: the ARM domain is auto-inhibitory, SAM-SAM domain interactions mediate multimerization, and the TIR domain has intrinsic NAD+ hydrolase activity that precipitates axonal demise. Whether and how these distinct functions contribute to TLR signaling is unknown. Here we show divergent signaling requirements for dSARM in injury-induced axon degeneration and TLR-mediated developmental glial phagocytosis through analysis of new knock-in domain and point mutations. We demonstrate intragenic complementation between reciprocal pairs of domain mutants during development, providing evidence for separability of dSARM functional domains in TLR signaling. Surprisingly, dSARM's NAD+ hydrolase activity is strictly required for both degenerative and developmental signaling, demonstrating that TLR signal transduction requires dSARM's enzymatic activity. In contrast, while SAM domain-mediated dSARM multimerization is important for axon degeneration, it is dispensable for TLR signaling. Finally, dSARM functions in a linear genetic pathway with the MAP3K Ask1 during development but not in degenerating axons. Thus, we propose that dSARM exists in distinct signaling states in developmental and pathological contexts.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.