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Fig. 7. Foxp2-/-;Foxp1+/- mutants have
defects in esophageal muscle development. (A-F) Esophageal
development was examined by Hematoxylin and Eosin staining in wild-type (A,B),
Foxp2-/- mutant (C,D) and
Foxp2-/-;Foxp1+/- mutant (E,F) mice at E18.5.
As early as E14.5, the smooth muscle surrounding the esophagus was thinner in
Foxp2-/-;Foxp1+/- mutants than in either
Foxp2-/- or wild-type littermates (A,C,E). By E18.5,
Foxp2-/-;Foxp1+/- mutants had severely dilated
esophagi with a very thin muscular layer (B,D,F). (G-J) Smooth muscle
actin (sm 
-actin) staining revealed a single muscular layer surrounding
Foxp2-/-;Foxp1+/- esophagi as compared with
wild-type animals (black arrowheads). This single muscular layer also appeared
thicker in Foxp2-/-;Foxp1+/- mutants (I,J). The
sm-actin-positive submucosal layer was unchanged in
Foxp2-/-;Foxp1+/- mutants (white arrowheads).
(K,L) MyoD immunohistochemistry demonstrated the presence of
skeletal muscle in the esophagi of wild-type embryos (K, arrowheads) and
revealed a lack of skeletal muscle contribution to
Foxp2-/-;Foxp1+/- esophagi (L). Scale bars: 100
µm in A-F; 50 µm in G-L.
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