FTO influences adipogenesis by regulating mitotic clonal expansion

Myrte Merkestein, Samantha Laber, Fiona McMurray, Daniel Andrew, Gregor Sachse, Jeremy Sanderson, Mengdi Li, Samuel Usher, Dyan Sellayah (), Frances M. Ashcroft () and Roger D. Cox ()
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Myrte Merkestein: MRC Harwell, Mammalian Genetics Unit
Samantha Laber: MRC Harwell, Mammalian Genetics Unit
Fiona McMurray: MRC Harwell, Mammalian Genetics Unit
Daniel Andrew: MRC Harwell, Mammalian Genetics Unit
Gregor Sachse: Anatomy and Genetics, University of Oxford
Jeremy Sanderson: MRC Harwell, Mammalian Genetics Unit
Mengdi Li: MRC Harwell, Mammalian Genetics Unit
Samuel Usher: Anatomy and Genetics, University of Oxford
Dyan Sellayah: MRC Harwell, Mammalian Genetics Unit
Frances M. Ashcroft: Anatomy and Genetics, University of Oxford
Roger D. Cox: MRC Harwell, Mammalian Genetics Unit

Nature Communications, 2015, vol. 6, issue 1, 1-9

Abstract: Abstract The fat mass and obesity-associated (FTO) gene plays a pivotal role in regulating body weight and fat mass; however, the underlying mechanisms are poorly understood. Here we show that primary adipocytes and mouse embryonic fibroblasts (MEFs) derived from FTO overexpression (FTO-4) mice exhibit increased potential for adipogenic differentiation, while MEFs derived from FTO knockout (FTO-KO) mice show reduced adipogenesis. As predicted from these findings, fat pads from FTO-4 mice fed a high-fat diet show more numerous adipocytes. FTO influences adipogenesis by regulating events early in adipogenesis, during the process of mitotic clonal expansion. The effect of FTO on adipogenesis appears to be mediated via enhanced expression of the pro-adipogenic short isoform of RUNX1T1, which enhanced adipocyte proliferation, and is increased in FTO-4 MEFs and reduced in FTO-KO MEFs. Our findings provide novel mechanistic insight into how upregulation of FTO leads to obesity.

Date: 2015
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DOI: 10.1038/ncomms7792

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