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Contribution of retinoic acid receptor gamma to retinoid‐induced craniofacial and axial defects

Exogenous retinoic acid (RA) administered during mouse embryogenesis can alter the pattern of the axial skeleton during two developmental periods: an early window (7 to 8.5 days post‐coitum; dpc) and a late window (9.5 to 11.5 dpc). Treatment during the early window results in vertebral homeotic transformations (predominantly posteriorizations) concomitant with rostral shifts in Hox gene expression, while treatment at the later window results in similar transformations without detectable alterations in Hox gene expression patterns. Mice null for retinoic acid receptor gamma (RARγ) exhibit axial defects, including homeosis of several vertebrae, therefore establishing a role for this receptor in normal axial specification. RARγ null mutants are also completely resistant to RA‐induced spina bifida, which occurs in wildtype embryos treated at 8.5–9.0 dpc, suggesting that this receptor specifically transduces at least a subset of the teratogenic effects of retinoids.