VITAMIN-A-DEFICIENCY AND THE EXPRESSION OF RETINOIC ACID RECEPTORS DURING EARLY CARDIOGENESIS IN QUAIL EMBRYO

The vitamin A deficiency-associated lethal syndrome observed in avian embryos may be linked to dysfunction of vitamin A-dependent genes. We tested this hypothesis in a quail embryo model by examining the expres sion of retinoic acid receptors (RARs) and cytosolic retinoic acid bin ding protein (CRABP) in normal and vitamin A-deficient embryos during early development. RAR alpha and RAR gamma mRNA were expressed at the same level in normal and vitamin A-deficient embryos during all stages studied. Expression of CRABP I was low in normal and vitamin A-defici ent quail embryos during early development, but increased rapidly at l ater stages. Two transcripts of RAR beta, 3.2 and 3.5 kb, were detecte d in quail embryos during developmental stages 6-12. In normal emryos the level of the 3.2-kb isoform increased as embryonic development adv anced. The expression of the 3.5-kb transcript was significantly decre ased in vitamin A-deficient embryos, while the 3.2-kb transcript was u ndetectable by northern analysis. In situ hybridization of stage 7-8 n ormal quail embryos using a chicken RAR beta 2 riboprobe revealed that RAR beta 2 expression was predominantly associated with the cell popu lations in heart-forming regions, somites, neural folds, notochord and the presumptive thyroid. In stark contrast, in the vitamin A-deficien t quail embryo RARP2 was not expressed in any of the above cell popula tions. We conclude that the expressions of RAR beta and CRABP I are de velopmentally regulated. Additionally, the expression of RAR beta 2 du ring early embryogenesis is regulated by vitamin A status. We propose that RARP2 plays an important role in the mechanism of action of retin oids in early avian development. The lack of expression of RAR beta 2 may be linked to abnormalities of the cardiovascular system.