RhoGDIβ favors SM-like cell fate via phospho-MLC-dependent actin reorganization. C3H10T1/2 cells were plated at 30% confluence and treated with or without BMP4 until post-confluence. A, F-actin in the cells with different treatments was stained with rhodamine-conjugated phalloidin and visualized by confocal laser-scanning microscopy. Bar = 10 μm. B, constitutively active Rac1 disrupted the stress fibers formed by RhoGDIβ overexpression. Bar = 10 μm. C, BMP4 inhibits the phosphorylation of MLC and cofilin. Phosphorylation of MLC and cofilin was revealed by Western blotting. β-Actin was used as a loading control. D, phosphorylation of MLC and cofilin in cells infected with RhoGDIβ or co-infected with RhoGDIβ and RacV12, which were plated at 30% confluence and treated with or without BMP4 until post-confluence. Phosphorylation of MLC and cofilin was revealed by Western blotting.