Evidence map›Paper›PMID 35737728›Full record

ArticlePLoS genetics2022

Distinct developmental and degenerative functions of SARM1 require NAD+ hydrolase activity.

E J Brace, Kow Essuman, Xianrong Mao, John Palucki, Yo Sasaki, Jeff Milbrandt, Aaron DiAntonio

Open access · goldAbstract read
In one paragraph

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 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.6field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. SARM1-Dependent Axon Degeneration: Nucleotide Signaling, Neurodegenerative Disorders, Toxicity, and Therapeutic Opportunities.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. A nerve-wracking buzz: lessons fromFrontiers in aging neuroscience · 2023
    Review
  9. Article
  10. Multifaceted roles of SARM1 in axon degeneration and signaling.Frontiers in cellular neuroscience · 2022
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

E J BraceDepartment of Developmental Biology, Washington University School of Medicine, St. Louis, Missouri, United States of America.
Kow EssumanDepartment of Genetics, Washington University School of Medicine, St. Louis, Missouri, United States of America.ORCID 0000-0002-6781-7248
Xianrong MaoDepartment of Genetics, Washington University School of Medicine, St. Louis, Missouri, United States of America.ORCID 0000-0003-0449-2164
John PaluckiDepartment of Developmental Biology, Washington University School of Medicine, St. Louis, Missouri, United States of America.
Yo SasakiDepartment of Genetics, Washington University School of Medicine, St. Louis, Missouri, United States of America.ORCID 0000-0003-0024-0031
Jeff MilbrandtDepartment of Genetics, Washington University School of Medicine, St. Louis, Missouri, United States of America.
Aaron DiAntonioDepartment of Developmental Biology, Washington University School of Medicine, St. Louis, Missouri, United States of America.ORCID 0000-0002-7262-0968
Washington University in St. Louis · US

Funding

Washington University Nutrition Obesity Research CenterP30DK056341 · NIDDK · WASHINGTON UNIVERSITY · PI Brian N Finck · 1999 to 2026
$30.2M
DISSECTION OF SARM1-INDUCED AXON DEGENERATION AND CELL DEATHR01NS087632 · NINDS · WASHINGTON UNIVERSITY · PI Aaron Diantonio, JEFFREY D MILBRANDT · 2014 to 2026
$6.4M
Regulation of axonal degeneration by the DLK kinaseR37NS065053 · NINDS · WASHINGTON UNIVERSITY · PI Aaron Diantonio · 2020 to 2026
$4.3M
REGULATION OF AXONAL DEGENERATION BY THE DLK KINASER01NS065053 · NINDS · WASHINGTON UNIVERSITY · PI DIANTONIO, AARON · 2010 to 2019
$3.3M
Regulating NAD Metabolism to Inhibit Axon Degeneration in Neurodegenerative DiseasesRF1AG013730 · NIA · WASHINGTON UNIVERSITY · PI MILBRANDT, JEFFREY D · 2017 to 2017
$2.8M
(PQ#9) Promoting Axon Stability to Prevent Therapy-induced Peripheral NeuropathyR01CA219866 · NCI · WASHINGTON UNIVERSITY · PI DIANTONIO, AARON, MILBRANDT, JEFFREY D · 2017 to 2021
$2.3M
NCI NIH HHS R01 CA219866NIA NIH HHS RF1 AG013730NIDDK NIH HHS P30 DK056341NINDS NIH HHS R01 NS065053NINDS NIH HHS R01 NS087632NINDS NIH HHS R37 NS065053
6 · The paper itself

Abstract

SARM1 is the founding member of the TIR-domain family of NAD+ hydrolases and the central executioner of pathological axon degeneration. SARM1-dependent degeneration requires NAD+ hydrolysis. Prior to the discovery that SARM1 is an enzyme, SARM1 was studied as a TIR-domain adaptor protein with non-degenerative signaling roles in innate immunity and invertebrate neurodevelopment, including at the Drosophila neuromuscular junction (NMJ). Here we explore whether the NADase activity of SARM1 also contributes to developmental signaling. We developed transgenic Drosophila lines that express SARM1 variants with normal, deficient, and enhanced NADase activity and tested their function in NMJ development. We find that NMJ overgrowth scales with the amount of NADase activity, suggesting an instructive role for NAD+ hydrolysis in this developmental signaling pathway. While degenerative and developmental SARM1 signaling share a requirement for NAD+ hydrolysis, we demonstrate that these signals use distinct upstream and downstream mechanisms. These results identify SARM1-dependent NAD+ hydrolysis as a heretofore unappreciated component of developmental signaling. SARM1 now joins sirtuins and Parps as enzymes that regulate signal transduction pathways via mechanisms that involve NAD+ cleavage, greatly expanding the potential scope of SARM1 TIR NADase functions.

Indexed as

Armadillo Domain ProteinsNADAnimalsAxonsCytoskeletal ProteinsDrosophilaNAD+ NucleosidaseArmadillo Domain ProteinsCytoskeletal ProteinsNADNAD+ Nucleosidase

Identifiers

PMID35737728
PMCPMC9223315
OpenAlexW4283375673

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.