ArticleNucleic acids research2020
O-GlcNAc regulates gene expression by controlling detained intron splicing.
Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 2 of them syntheses that pooled it.
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Who cites it
73 citing papers in PubMed, 2 syntheses or guidelines pooled it, 118 citations in OpenAlex.
- Tools for investigating O-GlcNAc in signaling and other fundamental biological pathways.The Journal of biological chemistry · 2024Pooled it
- The human O-GlcNAcome database and meta-analysis.Scientific data · 2021Pooled it
- Loss of O-GlcNAc transferase activity impairs the dynamic formation of protective stress granules in ischemic cardiomyocytes.The Biochemical journal · 2026Article
- Chemical biology tools for the O-GlcNAc modification: Determining systems-level functions and druggability.Current opinion in chemical biology · 2026Review
- Functional analysis of O-GlcNAcylation by networking of OGT interactors and substrates.Nature chemical biology · 2026Article
- Review
- Intron Retention as a Homeostatic State Variable for Drug Response and Recovery: Lessons from Depression for Broader Applications.International journal of molecular sciences · 2026Review
- The IR-Homeostat Hypothesis: Intron Retention as an Evolutionarily Conserved Fine-Tuning Layer and a Reversible Blood Biomarker of Homeostatic Dysregulation in Mood Disorders.International journal of molecular sciences · 2026Review
- Alternative splicing in cancer drug resistance: Mechanisms and therapeutic prospects (Review).Oncology reports · 2026Review
- Small molecule splicing modulators that disrupt O-GlcNAc homeostasis.Nature communications · 2026Article
- Human O-GlcNAcase catalytic-stalk dimer anchors flexible histone binding domains.Communications chemistry · 2025Article
- Protein O-GlcNAcylation in Health and Diseases.MedComm · 2025Review
- Dissecting the Mechanisms Underlying Substrate Recognition and Functional Regulation of O-GlcNAc Cycling Enzymes.ACS chemical biology · 2025Review
- A Genetically Encoded Assay System to Quantify O-GlcNAc Transferase (OGT) Activity in Live Cells.Angewandte Chemie (International ed. in English) · 2025Article
- Next-Generation Mapping of the ACINUS-Mediated Alternative Splicing Machinery and Its Regulation by O-glycosylation inbioRxiv : the preprint server for biology · 2025Article
- O-GlcNAcylation of nuclear proteins in the mouse liver exhibit daily oscillations that are influenced by meal timing.PLoS biology · 2025Article
- Protein O-GlcNAcylation in reproductive biology and the impact of metabolic disease.Human reproduction update · 2025Review
- An alternative cytoplasmic SFPQ isoform with reduced phase separation potential is up-regulated in ALS.Science advances · 2025Article
- O-GlcNAc modulation of nuclear pore complexes orchestrates mRNA export efficiency.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- OGT prevents DNA demethylation and suppresses the expression of transposable elements in heterochromatin by restraining TET activity genome-wide.Nature structural & molecular biology · 2025Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Intron detention in precursor RNAs serves to regulate expression of a substantial fraction of genes in eukaryotic genomes. How detained intron (DI) splicing is controlled is poorly understood. Here, we show that a ubiquitous post-translational modification called O-GlcNAc, which is thought to integrate signaling pathways as nutrient conditions fluctuate, controls detained intron splicing. Using specific inhibitors of the enzyme that installs O-GlcNAc (O-GlcNAc transferase, or OGT) and the enzyme that removes O-GlcNAc (O-GlcNAcase, or OGA), we first show that O-GlcNAc regulates splicing of the highly conserved detained introns in OGT and OGA to control mRNA abundance in order to buffer O-GlcNAc changes. We show that OGT and OGA represent two distinct paradigms for how DI splicing can control gene expression. We also show that when DI splicing of the O-GlcNAc-cycling genes fails to restore O-GlcNAc homeostasis, there is a global change in detained intron levels. Strikingly, almost all detained introns are spliced more efficiently when O-GlcNAc levels are low, yet other alternative splicing pathways change minimally. Our results demonstrate that O-GlcNAc controls detained intron splicing to tune system-wide gene expression, providing a means to couple nutrient conditions to the cell's transcriptional regime.
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Registered trials
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.