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O-GlcNAc cycling: emerging roles in development and epigenetics Love DC; Krause MW; Hanover JASemin Cell Dev Biol 2010[Aug]; 21 (6): 646-54The nutrient-sensing hexosamine signaling pathway modulates the levels of O-linked N-acetylglucosamine (O-GlcNAc) on key targets impacting cellular signaling, protein turnover and gene expression. O-GlcNAc cycling may be deregulated in neurodegenerative disease, cancer, and diabetes. Studies in model organisms demonstrate that the O-GlcNAc transferase (OGT/Sxc) is essential for Polycomb group (PcG) repression of the homeotic genes, clusters of genes responsible for the adult body plan. Surprisingly, from flies to man, the O-GlcNAcase (OGA, MGEA5) gene is embedded within the NK cluster, the most evolutionarily ancient of three homeobox gene clusters regulated by PcG repression. PcG repression also plays a key role in maintaining stem cell identity, recruiting the DNA methyltransferase machinery for imprinting, and in X-chromosome inactivation. Intriguingly, the Ogt gene resides near the Xist locus in vertebrates and is subject to regulation by PcG-dependent X-inactivation. OGT is also an enzymatic component of the human dosage compensation complex. These 'evo-devo' relationships linking O-GlcNAc cycling to higher order chromatin structure provide insights into how nutrient availability may influence the epigenetic regulation of gene expression. O-GlcNAc cycling at promoters and PcG repression represent concrete mechanisms by which nutritional information may be transmitted across generations in the intra-uterine environment. Thus, the nutrient-sensing hexosamine signaling pathway may be a key contributor to the metabolic deregulation resulting from prenatal exposure to famine, or the 'vicious cycle' observed in children of mothers with type-2 diabetes and metabolic disease.|*Epigenesis, Genetic[MESH]|*Morphogenesis[MESH]|Acetylglucosamine/*metabolism[MESH]|Animals[MESH]|Biological Evolution[MESH]|Hexosamines/biosynthesis[MESH]|Homeodomain Proteins/genetics/metabolism[MESH]|Humans[MESH]|N-Acetylglucosaminyltransferases/genetics/metabolism[MESH]|Promoter Regions, Genetic[MESH]|Signal Transduction/physiology[MESH] |
