Fig. 4

Inhibition of BMP signaling during gastrulation results in decreased cardiomyocyte numbers. (A–C) Lateral views of embryos exposed to dorsomorphin from 50% epiboly (B) or tailbud (C) stages until 48 h.p.f.; all images are at the same magnification. (B) Embryos treated with dorsomorphin from 50% epiboly onward lack the ventral tail fin (arrowheads), phenocopying the laf mutant body morphology. (C) Embryos treated with dorsomorphin from tailbud stage onward display mild abnormalities of the ventral tail fin (arrowheads), which is smaller in comparison to control embryos (A, arrowheads) treated with the same concentration of DMSO. (D) Quantification of cardiomyocyte number at 48 h.p.f. following dorsomorphin treatment. Graph as in Fig. 1; see also Table S2. n = 10 for control DMSO treatment, n = 10 for 50% epiboly treatment, n = 11 for tailbud treatment. (E) Quantification of cardiomyocyte number at 48 h.p.f., following heat shock of embryos carrying the transgene Tg(hsp701:dnBmpr-GFP). Control embryos were non-transgenic siblings, and heat shocks were performed at 65% epiboly, 75% epiboly, and the 8-somite stage. Graph as in Fig. 1; see also Table S3. n = 18 for non-transgenic embryos, n = 14 for heat shock at 65% epiboly, n = 17 for heat shock at 75% epiboly, and n = 17 for heat shock at the 8-somite stage. Statistically significant differences from wild-type are indicated by asterisks (p < 0.005) or carets (p < 0.05). Differences observed between the effects of dorsomorphin exposure and heat shock may be explained by differences in the strength of inhibition provided by each method.