Fig. 2

Fig. 2 Genetic mapping and identification of the headfish mutation. (A) The hdf locus is roughly mapped in the middle of medaka LG9, near the EST marker OLb0402d. (B) Structure of FGFR1 and its corresponding exons. Medaka fgfr1 consists of at least 20 exons. A G-to-C point mutation was found in exon 6, indicated by a red asterisk. The mutation causes an amino acid substitution W181C in the second immunoglobulin (IG) domain. (C) The mutated tryptophan residue is conserved among all of the FGFRs from Drosophila to human, indicating its essential role for the FGFR function. (D–G) Morpholino knock-down of fgfr1. Dorsal views of the trunk (D, E) and head (F, G) regions of control (D, F) and morphant (E, G) embryos are shown. Note that MO injection phenocopies hdf mutants. Anterior to the left. (H–J) Rescue of the mutant phenotype by injection of RNA encoding wild-type Fgfr1. Oblique dorsal views of the trunk region of control (H), hdf mutant (I) and RNA-injected hdf mutant (J) are shown. Note that the injected hdf mutant forms somites (J). Anterior to the left. (K–M) Responsiveness to exogenous FGFs. Mid-gastrula embryos transplanted with FGF8-beads on the dorsal side were stained with sprouty4 probe. Lateral views of wild-type (K), hdf mutant (L) and control wild-type (M) embryos are shown. Animal pole to the top. The control embryo was transplanted with a BSA-soaked bead (M). In addition to endogenous expression in the marginal and dorsal mesoderm, sprouty4 expression is induced around the FGF8-beads (K), whereas the FGF8-beads fail to induce sprouty4 in the hdf mutant (L).