Fig. 2

Loss of chordino has no apparent effect on gene expression in swirl (swr) and snh embryos. msxB expression at the 5-somite stage (A–D). (A) Wild type. (B) din embryos exhibit a variable reduction of anterior msxB staining in the presumptive neural crest (nc). (C and D) A similar small range of msxB expression in an anterior ventral position (arrowhead) is observed in embryos from both swirl single heterozygous and swirl;din double heterozygous crosses: shown here are weak (C) and strong (D) phenotypes. Expression of foxd3 (formerly fkd6) in the neural crest progenitors in 5-somite stage snh mutants is not affected by loss of din (E–H, lateral views, dorsal to the right; insets are dorsal-anterior views with anterior to the left). (E) Expression of foxd3 in the prospective cranial neural crest (bracket) and pax2.1 in the mid/hindbrain boundary (white box in inset) of a wild type embryo. (F) din mutant embryos exhibit a variable decrease in the width of anterior neural tissue as seen by decreased spacing between the domains of foxd3 expression and the width of the mid/hindbrain boundary. (G and H) The range of expanded foxd3 expressing neural crest phenotypes observed in snh^ty68a embryos. The degree of expansion was unaffected by din genotype; both embryos shown are homozygous mutant for din as well as snh^ty68a. Classification of the embryos as either strong, moderate or weak snh mutant phenotypes (G is weak, H is strong), followed by examination of the din genotype revealed the following: strong, 4 din/din, 4 din/+; moderate, 3 din/din, 3 din/+, 4 +/+; weak 2 din/din, 3 +/+. In crosses with ogon, 1 of 5 embryos with a strong snh phenotype was homozygous mutant for ogon. Of 4 embryos with a weak snh phenotype, none was homozygous mutant for ogon (data not shown).