Fig. 2: SMAD2/3-dependent TGFβ signalling does not regulate myogenic differentiation in vivo.
From: TGFβ signalling acts as a molecular brake of myoblast fusion
a–c, e–g, i–k Dorsal views of confocal stacks of somites observed at E4.5. To test myogenic differentiation, they were electroporated in the DML at E2.5 with the ubiquitous (CAGGS) promoter (b, f, j) or the muscle specific MLC promoter (c, g, k) driving expression of SMAD3 (b, c), TGFBR2 (f, g) and DN TGFBR1 (j, k). (CAGGS empty vector as control). They were also co-electroporated with two plasmids, CAGGS RFP (red) and MLC GFP (green) that label all electroporated cells or only myocytes, respectively; in blue, MyHC staining. d, h, l Scatter plots graphs showing the ratio of myocytes generated from the electroporated DML progenitors in each conditions. Statistical analyses: CAGGS SMAD3: \(\bar x\): 1.25; n = 24; CAGGS SMAD3 vs Ctrl, Mann–Whitney non-parametric test: P-value: 0.71; MLC SMAD3: \(\bar x\): 1.27; n = 19; P-value: 0.32; Ctrl: \(\bar x\): 1.16; n = 13. CAGGS TGFBR2: \(\bar x\): 1.46; n = 24; P-values: 0.99; MLC TGFBR2: \(\bar x\): 1.15; n = 11; P-value: 0.38; Ctrl: \(\bar x\): 1.37; n = 25. CAGGS DN TGFBR1: \(\bar x\): 1.03; n = 28; P-value: 0.86; MLC DN TGFBR1: \(\bar x\): 1.13; n = 3; P-value: 0.19; Ctrl: \(\bar x\): 1.01; n = 39. In d, h, l means and standard deviation are indicated; ns: non statistically significant difference. Source data are provided (see ‘Data availability’).
