Fig. 2. Neural crest cells migrate into the presumptive FNP despite exposure to RAR/RXR antagonists. (A) Quail donor neural crest cells from the forebrain (f) and midbrain (m), when transplanted orthotopically to chick host embryos between stage 9 and stage 10^–, give rise to components of the FNP (fn), as shown schematically (B) in a lateral view of the avian head skeleton (based on similar drawings by Noden, 1987). (C) In sagittal sections of chimeric embryos at stage 36, quail donor neural crest cells are found throughout chick host FNP-derived tissues, but not in the maxillary (mx) or mandibular (ma) processes (n=6). In an area of nasal capsule cartilage (boxed, shown at higher magnification in D), quail neural crest-derived cells appear black and are completely integrated into the host structures. Cartilage of mixed chick host and quail donor origin can be observed (arrows). Quail donor neural crest cells were transplanted into chick host embryos between stage 9 and stage 10^–, and then exposed 2-4 hours later at stage 10 to DMSO control beads (E, asterisk) or RAR/RXR antagonist beads (F, asterisk). After 24 hours, transplanted cells are integrated into the neuroepithelium above the lumen of the forebrain (f) and also have migrated into the FNP (fn; arrows) as shown in sagittal sections (n=7). Embryos were also exposed to RAR/RXR antagonists at stage 10, and immediately thereafter neural crest cells from the forebrain (f) and midbrain (m) were labeled with DiI. Twenty-four hours later, we observe DiI labeled cells in the presumptive FNP of control (G) and treated (H) embryos, which demonstrates that the neural crest still migrates into the region despite treatment with RAR/RXR antagonists (n=7). Scale bars: 1 mm in C; 100 µm in D; 200 µm in E-H.