Fig. 7. Reduction of AER-FGF dose rescues syndactyly in Msx2-Cre; Bmpr1a^flox/null mouse forelimbs. (A-F) Dorsal view of forelimbs (anterior to left) of the genotype shown. Interdigital webbing occurs owing to Msx2-Cre-mediated inactivation of Bmpr1a (B), even when Fgf8 is also inactivated (C). However, note that loss of Bmpr1a rescues the hypodactyly phenotype due to Msx2-Cre-mediated inactivation of Fgf8 (C) (also see Fig. 6). (D) Inactivation of one copy of Fgf8 partially rescues webbing in Msx2-Cre; Bmpr1A^flox/null forelimbs.(E,F) Inactivation of one copy of Fgf4 mostly rescues webbing in Msx2-Cre; Bmpr1A^flox/null;Fgf8^flox/null forelimbs, as well as restoring the hypodactyly phenotype resulting from loss of Fgf8. The inset in F is a skeletal preparation showing hypodactyly and a missing phalange (^*). All animals were approximately 8 weeks of age, except for that in E which was 3 months of age, which accounts for the longer nails of this limb. Note that owing to Msx2-Cre expression in the hair follicle (Pan et al., 2004), Msx2-Cre; Bmpr1a^flox/null animals (B-F) have a hair phenotype.