Mechanistically, this is mediated by an insulin-dependent overgrowth that arises from histone deacetylase (HDAC)-dependent β-cell hyperproliferation. We find that Nnat deficiency in isogenic mice triggers the emergence of a bi-stable polyphenism, where littermates emerge into adulthood either 'normal' or 'overgrown'. Here, we identify neuronatin (NNAT) as a conserved factor that buffers against UPV. The mechanisms that generate this 'unexplained' phenotypic variation (UPV) remain largely unknown. in genetically 'identical' individuals indicate that as much as 50% of complex trait variation cannot be traced to genetics or to the environment. 16 Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany. 15 Van Andel Institute, Grand Rapids, MI, USA.1 Van Andel Institute, Grand Rapids, MI, USA. 14 Helmholtz Institute for Metabolic, Obesity and Vascular Research (HI-MAG) of the Helmholtz Zentrum München at the University of Leipzig and University Hospital Leipzig, Leipzig, Germany.13 Microbiology and Cell Science Department, University of Florida, Gainesville, FL, USA.12 Institute for Integrative Systems Biology, Spanish National Research Council (CSIC), Paterna, Valencia, Spain.11 Genomic Medicine Center, Children's Mercy Research Institute, Children's Mercy Kansas City, MO, USA.10 Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark.9 Lund University Diabetes Centre, Lund University, Malmö, Sweden.8 Steno Diabetes Center Copenhagen, Herlev, Denmark.7 Department of Endocrinology, Rigshospitalet, Copenhagen, Denmark.6 Department of Neurodegenerative Science, Van Andel Institute, Grand Rapids, MI, USA.5 Roche Diagnostics Deutschland, Mannheim, Germany.4 Medical Faculty, University of Leipzig, University Hospital for Children & Adolescents, Center for Pediatric Research Leipzig, Leipzig, Germany.3 BioBam Bioinformatics, Valencia, Spain.2 Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany.1 Van Andel Institute, Grand Rapids, MI, USA.
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