Epigenetic ON/OFF Switches for Obesity

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Epigenetic ON/OFF Switches for Obesity Carmelo Quarta, Robert Schneider, Matthias H. Tschöp Cell Volume 164, Issue 3, Pages 341-342 (January 2016) DOI: 10.1016/j.cell.2016.01.006 Copyright © 2016 Elsevier Inc. Terms and Conditions

Figure 1 An ON/OFF Switch for Obesity Mutations in the chromatin-associated co-repressor Trim28/KAP1 (Trim28+/D9) affect the formation of a functional TRIM28-ZFP57 complex, which in turn affects chromatin states and modifications during embryonic development. Such (not yet identified) epigenetic alterations might be linked to a downregulated expression of an imprinted cluster of genes named IGN1. Reduced levels of components of the IGN1 network, including Nnat and Peg3, could lead to an obese-ON program. This program of obesity susceptibility is linked to a phenotypic switch in the body weight in adult genetically identical Trim28+/D9 mice, rendering them either normal or obese but without an intermediate phenotype. Such polyphenism might be influenced by environmental signals including dietary conditions, hormonal signaling, and changes in the environmental temperature, occurring in early life stages, during development, or potentially in the prior generation. Cell 2016 164, 341-342DOI: (10.1016/j.cell.2016.01.006) Copyright © 2016 Elsevier Inc. Terms and Conditions