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|Title:||The transcription factor SOX6 contributes to the developmental origins of obesity by promoting adipogenesis||Authors:||Ingham, Philip William
Leow, Melvin K. S.
Lee, Yung Seng
Ng, Kai Lyn
Leow, Shi Chi
Too, Peh Gek
Chong, Yap Seng
Gluckman, Peter D.
|Issue Date:||2016||Source:||Leow, S. C., Poschmann, J., Too, P. G., Yin, J., Joseph, R., McFarlane, C., Dogra, S., et al. (2016). The transcription factor SOX6 contributes to the developmental origins of obesity by promoting adipogenesis. Development, 143(6), 950-961. doi:10.1242/dev.131573||Series/Report no.:||Development||Abstract:||An association between impaired fetal growth and the postnatal development of obesity has been established. Here, by comparing adipocytes differentiated from mesenchymal stem cells (MSCs) taken from the umbilical cord and derived from normal and growth-restricted neonates, we identified the transcription factor SOX6 as highly expressed only in growth-restricted individuals. We found that SOX6 regulates adipogenesis in vertebrate species by activating adipogenic regulators including PPARγ, C/EBPα and MEST. We further show that SOX6 interacts with β-catenin in adipocytes, suggesting an inhibition of WNT/β-catenin signaling, thereby promoting adipogenesis. The upstream regulatory region of the MEST gene in MSCs from growth-restricted subjects harbors hypomethylated CpGs next to SOX6 binding motifs, and we found that SOX6 binding is impaired by adjacent CpG methylation. In summary, we report that SOX6 is a novel regulator of adipogenesis synergizing with epigenetic mechanisms.||URI:||https://hdl.handle.net/10356/89571
|ISSN:||0950-1991||DOI:||http://dx.doi.org/10.1242/dev.131573||Rights:||© 2016 The Author(s) (published by The Company of Biologists Ltd.). This paper was published in Development and is made available as an electronic reprint (preprint) with permission of The Author(s). (published by The Company of Biologists Ltd.). The published version is available at: [http://dx.doi.org/10.1242/dev.131573]. One print or electronic copy may be made for personal use only. Systematic or multiple reproduction, distribution to multiple locations via electronic or other means, duplication of any material in this paper for a fee or for commercial purposes, or modification of the content of the paper is prohibited and is subject to penalties under law.||Fulltext Permission:||open||Fulltext Availability:||With Fulltext|
|Appears in Collections:||LKCMedicine Journal Articles|
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