Fig. S6

DEAB treatment initiated at 24 hpf leads to partial restoration of mesenchymal gene expression in ring1b fin buds. (A) In situ hybridization for the RA-responsive genes dhrs3 (a-f) hoxc6a (g-l) and hoxc8a (m-r) in wild-type and ring1b embryos at 48 hpf, treated with DEAB from 24 hpf. DEAB (10 μM and 100 μM) potently suppresses expression of dhsr3 in wild-type and ring1b embryos (a-f). While 10 μM DEAB suppresses ectopic overexpression of hoxc6a and hoxc8a in ring1b embryos, 100 µM DEAB leads to more potent inhibition (i,k,o,q). (B) In situ hybridization for tbx5 (a-f), hand2 (g-l) and fgf24 (m-r) in wild-type and ring1b embryos at 40 hpf, treated with DEAB from 15 ss. Inhibition of RA signaling by DEAB leads to downregulation of tbx5 (c,e), hand2 (i,k) and fgf24 (o,q) expression in wild-type embryos in a dose-dependent manner. DEAB (10 μM) leads to almost complete downregulation of tbx5 expression in ring1b fin buds (d) and this effect is more pronounced with 100 μM DEAB (f). DEAB treatment initiated at 15 ss in ring1b embryos does not have an effect on the (lack of) expression of hand2 (j,l) and fgf24 (p,r) in ring1b fin buds. (C) In situ hybridization for tbx5 (a-f), hand2 (g-l) and fgf24 (m-r) in wild-type and ring1b embryos at 40 hpf, treated with DEAB from 24 hpf. DEAB treatment initiated at 24 hpf does not have a significant impact in expression of tbx5 (c,e), hand2 (i,k) and fgf24 (o,q) in wild-type fin buds. DEAB treatment of ring1b embryos initiated at 24 hpf leads to partial restoration of tbx5 (d,f) and hand2 (j,l) expression in a dose-dependent manner. However, this treatment does not lead to restoration of fgf24 expression (p,r).