ArticleProceedings of the National Academy of Sciences of the United States of America2006
Caenorhabditis elegans ortholog of a diabetes susceptibility locus: oga-1 (O-GlcNAcase) knockout impacts O-GlcNAc cycling, metabolism, and dauer.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.
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Who cites it
94 citing papers in PubMed, 161 citations in OpenAlex.
- PerturbingCells · 2026Article
- Human O-GlcNAcase catalytic-stalk dimer anchors flexible histone binding domains.Communications chemistry · 2025Article
- HumanResearch square · 2025Article
- O-GlcNAc transferase promotes synaptic assembly independent of catalytic activity inJournal of biosciences · 2025Article
- A Novel In Vivo Method UsingPharmaceuticals (Basel, Switzerland) · 2024Article
- Motif-dependent binding on the intervening domain regulates O-GlcNAc transferase.Nature chemical biology · 2023Article
- Nucleoporin foci are stress-sensitive condensates dispensable for C. elegans nuclear pore assembly.The EMBO journal · 2023Article
- Targeting protein modifications in metabolic diseases: molecular mechanisms and targeted therapies.Signal transduction and targeted therapy · 2023Review
- A novel binding site on the cryptic intervening domain is a motif-dependent regulator of O-GlcNAc transferase.Research square · 2023Article
- O-GlcNAc transferase plays a non-catalytic role in C. elegans male fertility.PLoS genetics · 2022Article
- Protein O-GlcNAcylation and the regulation of energy homeostasis: lessons from knock-out mouse models.Journal of biomedical science · 2022Review
- Inhibition of O-GlcNAcylation protects from Shiga toxin-mediated cell injury and lethality in host.EMBO molecular medicine · 2022Article
- Article
- A nexus of lipid andFrontiers in endocrinology · 2022Review
- Review
- Effector and regulator: Diverse functions of C. elegans C-type lectin-like domain proteins.PLoS pathogens · 2021Article
- Role of O-linked N-acetylglucosamine in the homeostasis of metabolic organs, and its potential links with diabetes and its complications.Journal of diabetes investigation · 2021Review
- Article
- O-GlcNAcylation as a Therapeutic Target for Alzheimer's Disease.Neuromolecular medicine · 2020Review
- O-GlcNAcylation and its role in the immune system.Journal of biomedical science · 2020Review
34 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
A dynamic cycle of O-linked N-acetylglucosamine (O-GlcNAc) addition and removal acts on nuclear pore proteins, transcription factors, and kinases to modulate cellular signaling cascades. Two highly conserved enzymes (O-GlcNAc transferase and O-GlcNAcase) catalyze the final steps in this nutrient-driven "hexosamine-signaling pathway." A single nucleotide polymorphism in the human O-GlcNAcase gene is linked to type 2 diabetes. Here, we show that Caenorhabditis elegans oga-1 encodes an active O-GlcNAcase. We also describe a knockout allele, oga-1(ok1207), that is viable and fertile yet accumulates O-GlcNAc on nuclear pores and other cellular proteins. Interfering with O-GlcNAc cycling with either oga-1(ok1207) or the O-GlcNAc transferase-null ogt-1(ok430) altered Ser- and Thr-phosphoprotein profiles and increased glycogen synthase kinase 3beta (GSK-3beta) levels. Both the oga-1(ok1207) and ogt-1(ok430) strains showed elevated stores of glycogen and trehalose, and decreased lipid storage. These striking metabolic changes prompted us to examine the insulin-like signaling pathway controlling nutrient storage, longevity, and dauer formation in the C. elegans O-GlcNAc cycling mutants. Indeed, we found that the oga-1(ok1207) knockout augmented dauer formation induced by a temperature sensitive insulin-like receptor (daf-2) mutant under conditions in which the ogt-1(ok430)-null diminished dauer formation. Our findings suggest that the enzymes of O-GlcNAc cycling "fine-tune" insulin-like signaling in response to nutrient flux. The knockout of O-GlcNAcase (oga-1) in C. elegans mimics many of the metabolic and signaling changes associated with human insulin resistance and provides a genetically amenable model of non-insulin-dependent diabetes.
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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.