Fig. 7
From: Meis2 is essential for cranial and cardiac neural crest development
Conditional inactivation of Meis2 in NCC affects osteochondrogenesis in the head. (a-a’) Illustration of the zone of Cre activity visualized in AP2α-Cre/ROSA26 embryos, left: transverse section of E10.5 embryo, right: sagittal view on E13.5. (b-b) Meis2 immnunostaining of AP2α-Cre/Meis2cKO embryos at E10.5, transverse sections in the region of hindbrain and the first pharyngeal arch. Compare the area of Meis2 deletion with a comparable cryosection from AP2α-Cre /Meis2 cKO/ROSA26 in the left panel (a). (c-c’) Sagittal sections from cKO at E14, hematoxylin-eosin (H&E) staining. Note the abnormal palate (p*) and tongue (t*). (d-d’) A higher magnification of the tongue on transverse sections at E14 documents its much reduced size and tissue disorganization. (e-e’) An example of severely disrupted palate (p*) in some cKO embryos, transverse section H&E staining. Alcian staining of cartilage at E16 with no otic capsule in cKO. (g-g’) Submandibular gland is almost absent and tongue muscle severed, transverse sections. (h-h’) Alizarin Red/Alcian Blue staining of E17.5 heads. Side view with remarkably shorter mandible (arrow), absent interparietal bone, abnormal hyoid bone and otic capsule cartilage. Ossification frontline of the parietal bone is severed in the mutants (arrowhead). (i-i’) Ventral views showing an abnormal hyoid bone (asterisk). oc, otic capsule cartilage; ip, interparietal bone; hy, hyoid bone; mb, mandible, p, palate; pr, parietal bone; smg, submandibular gland; t, tongue