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.