Published May 4, 2023 | Version Porcine-Adipose-paper
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Dynamic chromatin architecture of the porcine adipose tissues with weight gain and loss

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To identify the regulatory mechanisms of three-dimensional (3D) genome architecture underlying obesity phenotypes in anatomically distinct adipose tissues (ATs), we used an adult female miniature pig model with diet-induced weight gain/weight loss to generate 249 high-resolution in situ Hi-C chromatin contact maps of subcutaneous AT and three visceral ATs. Investigation of transcriptomic and chromatin architectural changes among the four ATs under different nutritional treatments showed multi-level remodeling of chromatin architecture that underpins transcriptomic divergence in ATs. These changes are potentially linked to progressive metabolic risks in obesity development (e.g., increasing inflammation) and the existence of persistent obesogenic memory even after caloric restriction-induced weight loss. Analysis of chromatin architecture among subcutaneous ATs of different mammals suggested the presence of transcriptional regulatory divergence that could be responsible for phenotypic, physiological, and functional differences in ATs. Analysis of regulatory element (enhancer) conservation in all four ATs in pigs and humans revealed similarities in the regulatory circuitry of genes responsible for the obesity phenotype and identified non-conserved elements in species-specific gene sets that underpin AT specialization. This work provides an integrated, data-rich tool for discovering obesity-related regulatory elements through comparison of the 3D genome architecture of humans and pigs.

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JiamanZhang/Lab_Porcine-Adiposes_paper_codes-Porcine-Adipose-paper.zip

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https://github.com/JiamanZhang/Lab_Porcine-Adiposes_paper_codes/tree/Porcine-Adipose-paper (URL)