Fig. 6. Double mutant analysis reveals that fgf8 genetically interacts with ntl and spt. Markers used for in situ hybridization and immunohistochemistry in A-E and K-N, as well as identifiers (e.g. arrows) are as described for Fig. 4A. Representative pictures of stained 12- to 13-somite-stage embryos (A-E,K-N) and live 24 hpf embryos (F-J,O-R) are shown. Relative to wild-type embryos (A), neither fgf8 (B) nor ntl (D) mutant embryos have severe deficiencies in the production of myod-expressing paraxial mesoderm (arrows), whereas fgf8;ntl double mutants (E) produce very little paraxial mesoderm and have significantly shorter tails at 24 hpf (J) in comparison with fgf8 (G) or ntl (I) single mutants. By contrast, fgf8;ntl double mutants appear to produce relatively normal amounts of pronephric tissue (E; asterisk). In addition to the single and double mutant phenotypes observed, fgf8^-;ntl^+/- embryos (C) produce less axial (Ntl expressing) and paraxial (myod expressing) mesoderm than do fgf8^-;ntl^+/+ embryos (B), and at 24 hpf (H) have tail lengths that are intermediate between embryos single mutant for either fgf8 (G) or ntl (I). Although neither fgf8 (L) nor spt (M) mutant embryos have severe deficiencies in the production of axial mesoderm, spt;fgf8 double mutant embryos produce a truncated notochord (N) and have shorter tails at 24 hpf (R) than either fgf8 (P) or spt (Q) single mutants. By contrast, spt;fgf8 double mutants appear to produce relatively normal amounts of pronephric tissue (N; asterisk).Wild-type sibling embryos (K,O) are shown for comparison. Scale bars: in A, 50 µm for A-E,K-N; in F, 100 µm for F-J,O-R.

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