Abstract
Brown adipose tissue (BAT) is important for thermoregulation via uncoupling of oxidative phosphorylation. In addition to BAT-driven thermogenesis, mammals use induced browning of subcutaneous white adipose tissue (scWAT) as a mechanism to cope with chronic cold stress. Under acute cold stress in mammals, JMJD1A, a histone H3 lysine 9 (H3K9) demethylase, upregulates thermogenic genes via β-adrenergic signaling in BAT through higher-order chromatin structural changes that occur independent of histone demethylase activity. Following exposure to chronic cold stress, scWAT browning occurs via a two-step process that requires both β-adrenergic-dependent phosphorylation of S265 and JMJD1A-induced demethylation of H3K9me2.
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