Fig. S2

Treatment with the RARα Antagonist Ro41-5253 (Lopez-Boado et al., 1996; Shibakura et al., 1997; Zhang et al., 1995) Phenocopies Treatment with More General Antagonists of RA Signaling, Suggesting that RARα Paralogs Are Required to Promote Forelimb Formation and Limit Cardiac Cell Number
(A and B, E and F) Expression patterns of rar parlogs at the tailbud stage; dorsal views, anterior to the top. (A and B) rarα paralogs (blue) (Hale et al., 2006; Waxman and Yelon, 2007) are expressed in posterior portions of LPM near raldh2 expression (redbrown) and therefore appear to be the best candidates for mediating RA signaling in FPs.
(E and F) rarγ paralogs (blue) are expressed more anteriorly and in the tailbud, farther from raldh2 expression.
(C and D, G and H) Treatment with RO causes phenotypes similar to those of embryos deficient in RA signaling, including pericardial edema and loss of pectoral fins; lateral views, anterior to the left, at 48 hpf, with higher magnification of pectoral fin outlined in (D and H).
(I and N) tbx5 expression at 30 hpf; dorsal views, anterior to the top. RO-treated embryos lack tbx5 expression in the pectoral fin bud mesenchyme.
(J–M and O–R) RO treatment does not affect retd expression at the tailbud stage, but reduces retd expression at the 8 somite stage; in contrast, RO treatment results in loss of hoxb5b expression at both the tailbud and 8 somite stages. Views are as presented in Figure 2. (S-b) RO treatment causes increases of atrial and ventricular cardiomyocyte populations comparable to those observed in DEAB-treated embryos; see also Tables S1 and S2. Views and graphs are as presented in Figure 1.