Abstract

Many findings indicate that active retinoids (vitamin A metabolites, which are known to be hormone-like ligands), are regulatory signals during embryogenesis. Treating early vertebrate embryos with retinoids can cause teratogenesis. Notably, it generates specific defects in the main body axis. Considering other data showing that early vertebrate embryos contain physiolocally relevant concentrations of endogenous active retinoids and express retinoid binding proteins and receptors, it is not unlikely that retinoids act as developmental signals, which regulate axial patterning in the early vertebrate embryo. The purpose of this review is to discuss this point, referring to retinoid teratogenesis, and to the availabilities and functions of retinoid ligands, biding proteins and receptors in the early embryo.

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