A new study from the Layne laboratory identified a function for the transcription factor FOXS1 in regulating TGFb-dependent changes in adipogenic differentiation: JBC in press.
White adipose tissue (WAT) fibrosis is a major determinant of obesity-induced dysfunction and is characterized by excessive extracellular matrix deposition and myofibroblast activation. In this study, first author Alexander Tavares and co-authors identified FOXS1, a member of the forkhead box transcription factor superfamily, as a transcriptional target of TGF-β1 signaling in primary human adipocyte stem cells. FOXS1 also attenuated the induction of several adipogenic factors and sensitized cells to the anti-adipogenic effects of TGF-β1. Furthermore, loss of endogenous FOXS1 improved adipogenic permissiveness and activated proadipogenic gene programs in progenitors, even after TGF-β1 stimulation. These results indicate that FOXS1 is a positive regulator of profibrotic TGF-β1-dependent cellular responses, orchestrating the regulation of molecular phenotypes that promote myofibroblast activation and block adipogenesis. Co-authors in this study from the Layne lab include Scott Connelly, Daryn Maksat, Jane Zheng and Nabil Rabhi from the Farmer lab.