Fig. S5

Inhibition of BMP signaling interferes with loss of cardiomyocyte differentiation markers and re-expression of a fetal form of myosin heavy chain. Related to Figure 6.

(A) Inhibition of BMP signaling either by treatment with 5 µM Dorsomorphin in myl7:GFP transgenic hearts or by noggin3 overexpression for 4 days in myl7:GFP; hsp70l:nog3 double transgenic hearts does not alter wound size (the ventricular area lacking GFP expression) at 7 dpi. Error bars represent SEM. Student’s t test, p = 0.49 (wild-type vs hsp70l:nog3), p = 0.23 (DMSO vs Dorsomorphin).

(B) Treatment of myl7:GFP transgenic fish with 5 µM Dorsomorphin for 4 days reduces the area of ventricular myosin heavy chain (Vmhc) expression in cardiomyocytes at 7 dpi. In processed Vmhc LUT images, all Vmhc signal with pixel intensity lower than 65 (8-bit image) were considered background. Error bars represent SEM. Scale bar, 50 µm. Student’s t test, p = 0.006.

(C) Immunofluorescence analysis reveals wound size at 21 dpi on heart sections of hsp70l:nog3; myl7:GFP (GFP+) and hsp70l:bmp2b (positive for myosin heavy chain staining) transgenics and their respective wild-type siblings subjected to the depicted heat-shock regime. Size of the wound tissue relative to the whole ventricle normalized to wild-type siblings is plotted. Error bars represent SEM. Student’s t test, p = 0.25 (nog3), p = 0.14 (bmp2b).