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PMID:16051707
| Citation |
Hanover, JA, Forsythe, ME, Hennessey, PT, Brodigan, TM, Love, DC, Ashwell, G and Krause, M (2005) A Caenorhabditis elegans model of insulin resistance: altered macronutrient storage and dauer formation in an OGT-1 knockout. Proc. Natl. Acad. Sci. U.S.A. 102:11266-71 |
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| Abstract |
O-linked N-acetylglucosamine (O-GlcNAc) is an evolutionarily conserved modification of nuclear pore proteins, signaling kinases, and transcription factors. The O-GlcNAc transferase (OGT) catalyzing O-GlcNAc addition is essential in mammals and mediates the last step in a nutrient-sensing "hexosamine-signaling pathway." This pathway may be deregulated in diabetes and neurodegenerative disease. To examine the function of O-GlcNAc in a genetically amenable organism, we describe a putative null allele of OGT in Caenorhabditis elegans that is viable and fertile. We demonstrate that, whereas nuclear pore proteins of the homozygous deletion strain are devoid of O-GlcNAc, nuclear transport of transcription factors appears normal. However, the OGT mutant exhibits striking metabolic changes manifested in a approximately 3-fold elevation in trehalose levels and glycogen stores with a concomitant approximately 3-fold decrease in triglycerides levels. In nematodes, a highly conserved insulin-like signaling cascade regulates macronutrient storage, longevity, and dauer formation. The OGT knockout suppresses dauer larvae formation induced by a temperature-sensitive allele of the insulin-like receptor gene daf-2. Our findings demonstrate that OGT modulates macronutrient storage and dauer formation in C. elegans, providing a unique genetic model for examining the role of O-GlcNAc in cellular signaling and insulin resistance. |
| Links |
PubMed PMC1183534 Online version:10.1073/pnas.0408771102 |
| Keywords |
Animals; Caenorhabditis elegans; Carmine/analogs & derivatives; DNA Primers; Disease Models, Animal; Fluorescent Antibody Technique; Glycogen/metabolism; Immunoblotting; Insulin Resistance/genetics; Larva/growth & development; Mutation/genetics; N-Acetylglucosaminyltransferases/genetics; Oxazines; Polymerase Chain Reaction; Signal Transduction/genetics; Trehalose/metabolism; Triglycerides/metabolism |
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Significance
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| Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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