Fig. 6.

Cooperative effects of FGF and BMP on thyroid specification. (A) Representative thyroid phenotypes recovered at 28 hpf by in situ hybridization of nkx2.4b and myl7 (cardiomyocytes) following HS treatment of double-transgenic Tg(hsp70l:bmp2b;hsp70l:ca-fgfr1) embryos at 20 hpf. Carriers of the individual transgenes were identified by genotyping. Note the expansion of the thyroidal nkx2.4b expression domain in embryos with concurrent overactivation of both pathways. (B) Top: Thyroid phenotypes recovered at 28 hpf after inhibition of FGF (8 µM PD166866) and BMP signaling (12 µM DMH1) from 10 to 24 hpf. Bottom: Rescue efficacy by concurrent overactivation of BMP or FGF signaling (repeated HS at 10, 15 and 20 hpf). Note that overactivation of BMP signaling could partially restore nkx2.4b expression in embryos treated with FGF inhibitor. Numbers indicate the proportion of embryos with the represented phenotype out of the total number of observed embryos and include carriers and non-carriers of the HS-inducible transgene. Dorsal views, anterior to the top. Hy, hypothalamus. Scale bars: 200 µm.