Function of vitamin A in vertebrate embryonic development

Advances in molecular biology and retinoic acid receptor research have sign ificantly contributed to the understanding of the role of vitamin A during vertebrate development. Examination of the function of this vitamin during very early developmental stages using the completely vitamin A-depleted avi an embryo has revealed that the vitamin A requirement begins at the time of formation of the primitive heart, circulation and specification of hindbra in. The lack of vitamin A at this critical time results in gross abnormalit ies and early embryonic death. In rodent models, vitamin A deficiency can b e targeted to later gestational windows and documents the need for vitamin A for more advanced stages of development. Major target tissues of Vitamin A deficiency include the heart, central nervous system and structures deriv ed from it, the circulatory, urogenital and respiratory systems, and the de velopment of skull, skeleton and limbs. These abnormalities are also eviden t in mice mutants from retinoid receptor knockouts; they have revealed both morphological and molecular aspects of vitamin A function during developme nt. Retinoic acid receptors (RAR) in partnership with retinoid X receptor ( RXR)alpha appear to be the important retinoid receptor transcription factor s regulating vitamin A function at the gene level during development via th e physiologic ligand all-trans-retinoic acid. Homeostasis of retinoic acid is maintained by developmentally regulated vitamin A metabolism enzyme syst ems. Inadequate vitamin A nutrition during early pregnancy may account for some pediatric congenital abnormalities.