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Fig. 7. Reduction of AER-FGF dose rescues syndactyly in Msx2-Cre;
Bmpr1aflox/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;
Bmpr1Aflox/null forelimbs.(E,F) Inactivation of one copy of
Fgf4 mostly rescues webbing in Msx2-Cre;
Bmpr1Aflox/null;Fgf8flox/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; Bmpr1aflox/null animals (B-F) have a hair
phenotype.
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