The following s01 nl subs2/15/2023 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. Studies in genetically ‘identical’ individuals indicate that as much as 50% of complex trait variation cannot be traced to genetics or to the environment. Nature Metabolism volume 4, pages 1150–1165 ( 2022) Cite this article Independent phenotypic plasticity axes define distinct obesity sub-types
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