Fig. 4.

Enhanced FGF signaling during late somitogenesis promotes thyroid precursor specification. (A) Distribution of thyroid phenotypes (nkx2.4b expression at 28 hpf) induced by overactivation of FGF signaling using HS treatment of Tg(hsp70l:ca-fgfr1) embryos at the indicated time points. Phenotypic data shown include carriers and non-carriers of the HS-inducible transgene. Cases with abnormal morphology/positioning of nkx2.4b expression domain are highlighted by dotted texture overlays. (B) Thyroid phenotypes recovered at 28 hpf by in situ hybridization of nkx2.4b and myl7 (cardiomyocytes) following overactivation of FGF signaling at the indicated time points. Arrow points to the thyroid anlage. 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 bar: 200 µm. (C) Total number of foregut endoderm cells expressing Pax2a (top) and cells expressing both Pax2a and YFP (bottom) following HS treatment of Tg(hsp70l:ca-fgfr1);Et(nkx2.4b:YFP) double-transgenic embryos at the indicated time points. Values for individual embryos and mean values (bars) are shown. Data shown include carriers and non-carriers of the HS-inducible transgene.