Fig. 1

Reduction of RA Signaling Causes an Increase in the Number of Atrial and Ventricular Cells

(A–C) Frontal views of hearts at 48 hpf expressing the transgene Tg(cmlc2:DsRed2-nuc) (red). Atria are labeled with the anti-Amhc antibody S46 (green). (B and C) Treatment with 1 μM DEAB or 10 μM BMS causes cardiac chamber enlargement.

(D) Mean and standard deviation (SD) of numbers of atrial and ventricular cardiomyocytes. Stages indicate when DEAB or BMS treatment was initiated. Asterisks indicate statistically significant differences relative to wild-type (p < 0.005).

(E) Fold difference in mean cell numbers relative to wild-type (WT) controls.

(F–I) Reduction of RA signaling causes increased expression of amhc and vmhc. Dorsal views, anterior to the top at the 20 or 22 somite stage.

(J) Mean and SD of areas of expression of amhc and vmhc in WT and BMS-treated embryos. Asterisks indicate statistically significant differences relative to WT (p < 0.005).

(K) Fold difference in mean areas of gene expression relative to WT controls.

(L and M) Schematic of 40% epiboly fate maps from WT and BMS-treated embryos indicating that the relative position of regions containing APs (green) and VPs (red) is unchanged when RA signaling is reduced. Percentages indicate the frequency of encountering APs or VPs in each region.

(N) Reduction of RA signaling increased the frequency of encountering VPs, but not APs, at 40% epiboly. The asterisk indicates statistically significant difference relative to WT (p < 0.005).

(O) Reduction of RA signaling increased the mean number of labeled progeny produced by APs but not VPs. The asterisk indicates statistically significant difference relative to WT (p < 0.05).