Early facial development in normal chick embryos was studied by scanning electron microscopy, and compared to the abnormal facial development of a mutant in which primary palate formation does not occur, thus resulting in bilateral cleft lip. In both normal and "cleft primary palate" mutant embryos, subsequent to the appearance of the nasal placodes, the surrounding tissues elevate to give rise to the presumptive facial primordia. As the facial primordia grow forward, they gradually assume the configuration of a square which is most pronounced at five days development. In normal embryos, the square configuration is then lost as the facial primordia become aligned in preparation for primary palate formation. The primary palate is formed at six days development by fusion of the "free-ended" medial nasal processes with the combined lateral nasal and maxillary processes across the nasal grooves. Just prior to fusion, long, slender filaments extend from the apposing surfaces of the facial primordia in the regions of prefusion contact. It is speculated that these "prefusion filaments" may function in alignment or adhesion of the facial primordia. In "cleft primary palate" embryos, facial morphogenesis appears to arrest at five days development, so that the square configuration persists. The medial nasal processes never contact the lateral nasal and maxillary processes, but instead remain separated from them by wide nasal grooves. Furthermore, facial primordia of mutant embryos do not exhibit the "prefusion filaments" characteristic of normal embryos.

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To determine whether inherited muscular dystrophy of the chicken is neurogenic or myogenic in origin, limb buds from homozygous normal and dystrophic chick embryos were exchanged prior to muscle differentiation and innervation. Biceps muscles of hatched chicks, in which muscle of the donor was innervated by nerves of the host, were analyzed for embryonic properties of muscle acetylcholinesterase and for fiber diameter, two distinctive markers for expression of the dystrophic gene. The results indicate that muscular dystrophy of the chicken is caused by an initial biochemical lesion in the limb and its muscle rather than in its innervating nerve.

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