In acute cold stress in mammals, JMJD1A, an H3K9 demethylase, up-regulates thermogenic gene expressions through -adrenergic signaling in brown adipose tissue (BAT). Aside BAT-driven thermogenesis, mammals also have another mechanism to cope with long-term cold stress by inducing the browning of subcutaneous white adipose tissue (scWAT). Here, we show that this occurs through a two-step process that requires both -adrenergic dependent phosphorylation of S265 and demethylation of H3K9me2 by JMJD1A. The histone demethylation independent acute Ucp1 induction in BAT and demethylation dependent chronic Ucp1 expression in beige-scWAT provide complementary molecular mechanisms to ensure an ordered transition between acute and chronic adaptation to cold stress. JMJD1A mediates two major signaling pathways, namlely -adrenergic receptor and PPAR activation, via PRDM16-PPAR-P-JMJD1A complex for beige adipogenesis. SOURCE: Juro Sakai (jmsakai-tky@umin.ac.jp) -  Research Center for Advanced Science and Technology, The University of Tokyo

Pluto Bioinformatics

GSE107900: RNA-sequence analysis of immortalized, differentiated preadipocytes derived from inguinal subcutaneous white adipose tissue.