Figure 5: PPARγ contributes to Mkl1 downregulation during adipocyte differentiation.

(a) The relative abundance of Mkl1 and Pparg mRNAs at the indicated times after exposure of DFAT cells to inducers of adipocytic differentiation was also determined. (a–c) P<0.05, (a–d) P<0.05, Tukey’s honest significant difference test. (b) DFAT cells stably expressing PPARγ (shPPARγ) or luciferase (shLuc, control) shRNAs were exposed to inducers of adipogenesis for 0 or 96 h and then assayed for the relative abundance of Pparg and Mkl1 mRNAs. The cells were also subjected to immunofluorescence analysis of PPARγ after 96 h. Nuclei were stained with Hoechst 33342. Scale bars, 100 μm. ND, not detected. (c) DFAT cells stably overexpressing PPARγ (PPARγ-OE) or infected with the corresponding empty vector (Mock) were assayed for the relative abundance of Pparg and Mkl1 mRNAs. *P<0.05, Student’s t-test. They were also subjected to immunofluorescence analysis of PPARγ expression. Nuclei were stained with Hoechst 33342. Scale bars, 100 μm. All quantitative data are means±s.d. (n=3 experiments). (d) Model for the regulation of adipocyte differentiation. Regulation of MKL1 by disruption of actin stress fibres drives adipocyte differentiation.