Evidence map›Paper›PMID 38843836›Full record

ArticleDevelopmental cell2024

Neuronal activity-driven O-GlcNAcylation promotes mitochondrial plasticity.

Seungyoon B Yu, Haoming Wang, Richard G Sanchez, Natasha M Carlson, Khanh Nguyen, Andrew Zhang, Zachary D Papich, Ahmed A Abushawish, Zachary Whiddon, Weronika Matysik and 7 more

Abstract read
In one paragraph

Article in Developmental cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Mitochondrial CaNature metabolism · 2026
    Article
  9. Article
  10. Review
  11. RNA triggers chronic stress during neuronal aging.bioRxiv : the preprint server for biology · 2025
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors.

Seungyoon B YuNeurobiology Department, School of Biological Sciences, University of California San Diego, La Jolla, CA 92093, USA.
Haoming WangNeurobiology Department, School of Biological Sciences, University of California San Diego, La Jolla, CA 92093, USA.
Richard G SanchezNeurobiology Department, School of Biological Sciences, University of California San Diego, La Jolla, CA 92093, USA.
Natasha M CarlsonNeurobiology Department, School of Biological Sciences, University of California San Diego, La Jolla, CA 92093, USA.
Khanh NguyenLaboratory for Immunochemical Circuits, Center of Autoimmunity and Inflammation, and Division of Signaling and Gene Expression, La Jolla Institute for Immunology, La Jolla, CA 92093, USA.
Andrew ZhangNeurobiology Department, School of Biological Sciences, University of California San Diego, La Jolla, CA 92093, USA.
Zachary D PapichNeurobiology Department, School of Biological Sciences, University of California San Diego, La Jolla, CA 92093, USA.
Ahmed A AbushawishNeurobiology Department, School of Biological Sciences, University of California San Diego, La Jolla, CA 92093, USA.
Zachary WhiddonNeurobiology Department, School of Biological Sciences, University of California San Diego, La Jolla, CA 92093, USA.
Weronika MatysikNeurobiology Department, School of Biological Sciences, University of California San Diego, La Jolla, CA 92093, USA.
Jie ZhangNeurobiology Department, School of Biological Sciences, University of California San Diego, La Jolla, CA 92093, USA.
Thomas C WhisenantCenter for Computational Biology and Bioinformatics, University of California San Diego, La Jolla, CA 92093, USA.
Majid GhassemianBiomolecular and Proteomics Mass Spectrometry Facility, University of California San Diego, La Jolla, CA 92093, USA.
John N KobersteinVollum Institute, Oregon Health & Science University, Portland, OR 97239, USA.
Melissa L StewartVollum Institute, Oregon Health & Science University, Portland, OR 97239, USA.
Samuel A MyersLaboratory for Immunochemical Circuits, Center of Autoimmunity and Inflammation, and Division of Signaling and Gene Expression, La Jolla Institute for Immunology, La Jolla, CA 92093, USA; Department of Pharmacology, Program in Immunology, and Moores Cancer Center, University of California San Diego, La Jolla, CA 92093, USA.
Gulcin PekkurnazNeurobiology Department, School of Biological Sciences, University of California San Diego, La Jolla, CA 92093, USA. Electronic address: gpekkurnaz@ucsd.edu.

Funding

UCSD/SDSU IRACDAK12GM068524 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI TREJO, JOANN · 2003 to 2025
$24.4M
GENETIC MECHANISMS AND REGULATIONT32GM007240 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HAMPTON, RANDOLPH Y. · 1985 to 2019
$23.8M
Pathways in Biological Sciences Training ProgramT32GM133351 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Matthew Daugherty, Randolph Y. Hampton · 2020 to 2026
$9.9M
Training in Multi-Scale Analysis of Biological Structure and FunctionT32EB009380 · NIBIB · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Andrew D. McCulloch, Padmini Rangamani · 2009 to 2026
$4.8M
NEUROBIOLOGY TRAINING PROGRAMT32NS007220 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI JIN, YISHI · 1985 to 2023
$4.5M
Metabolic Regulation of Mitochondrial FunctionR35GM128823 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Gulcin Pekkurnaz · 2018 to 2026
$4.1M
Elucidating the signaling and protein interaction networks of the O-GlcNAc transferase during embryonic stem cell state transitionsR35GM147554 · NIGMS · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI Samuel Anthony Myers · 2022 to 2026
$2.4M
NIBIB NIH HHS T32 EB009380NIGMS NIH HHS K12 GM068524NIGMS NIH HHS R35 GM128823NIGMS NIH HHS R35 GM147554NIGMS NIH HHS T32 GM007240NIGMS NIH HHS T32 GM133351NINDS NIH HHS T32 NS007220
6 · The paper itself

Abstract

Neuronal activity is an energy-intensive process that is largely sustained by instantaneous fuel utilization and ATP synthesis. However, how neurons couple ATP synthesis rate to fuel availability is largely unknown. Here, we demonstrate that the metabolic sensor enzyme O-linked N-acetyl glucosamine (O-GlcNAc) transferase regulates neuronal activity-driven mitochondrial bioenergetics in hippocampal and cortical neurons. We show that neuronal activity upregulates O-GlcNAcylation in mitochondria. Mitochondrial O-GlcNAcylation is promoted by activity-driven glucose consumption, which allows neurons to compensate for high energy expenditure based on fuel availability. To determine the proteins that are responsible for these adjustments, we mapped the mitochondrial O-GlcNAcome of neurons. Finally, we determine that neurons fail to meet activity-driven metabolic demand when O-GlcNAcylation dynamics are prevented. Our findings suggest that O-GlcNAcylation provides a fuel-dependent feedforward control mechanism in neurons to optimize mitochondrial performance based on neuronal activity. This mechanism thereby couples neuronal metabolism to mitochondrial bioenergetics and plays a key role in sustaining energy homeostasis.

Indexed as

AcetylglucosamineEnergy MetabolismMitochondriaN-AcetylglucosaminyltransferasesNeuronsAnimalsGlucoseHippocampusMiceMice, Inbred C57BLNeuronal PlasticityAcetylglucosamineGlucoseN-AcetylglucosaminyltransferasesATP synthesisglycosylationmitochondrianeuronal metabolismO-GlcNAc transferaseO-GlcNAcylationsynaptic activity

Identifiers

PMID38843836
PMCPMC11338717

What OpenQuestion holds

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Registered trials

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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.