Vitamin A and its derivatives, the retinoids, participate in formation
of diverse embryonic structures, including face, heart, eye, limb and
nervous system. Studies of retinoid-deficient and -treated embryos, a
nd of receptor null mutants, provide evidence that this participation
involves interactions between retinoids and their receptors. Targeted
retinoid application and retinoid deficiency, using in ovo avian embry
os, has identified early cardiogenic contributions, including cardiocy
te gene expression and differentiation, heart tube fusion and laterali
ty, and segmental identity, Also useful is a mammalian model, which ta
rgets retinoid deficiency to distinct gestational windows, circumventi
ng limitations of traditional deficiency studies and current null muta
nt technologies, Rat embryos made deficient in retinoids during gestat
ional d 11.5-13.5 exhibit specific cardiac, limb, ocular and nervous s
ystem deficits, That many of the anomalies previously reported in reti
noid receptor null mutants are observed in deficiency confirms that li
gand-receptor interactions are essential for embryonic development, Ot
her defects are novel, reemphasizing the functional redundancy of reti
noid receptors and that retinoid receptors have multiple and overlappi
ng contributions to morphogenesis.