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 expression of retinoic acid receptors (RARs) and cytosolic retinoic acid binding protein (CRABP) in normal and vitamin A-deficient embryos during early development. RARα and RARγ 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-deficient quail embryos during early development, but increased rapidly at later stages. Two transcripts of RARβ, 3.2 and 3.5 kb, were detected in quail embryos during developmental stages 6-12. In normal emryos the level of the 3.2-kb isoform increased as embryonic development advanced. The expression of the 3.5-kb transcript was significantly decreased in vitamin A-deficient embryos, while the 3.2-kb transcript was undetectable by northern analysis. In situ hybridization of stage 7-8 normal quail embryos using a chicken RARβ2 riboprobe revealed that RARβ2 expression was predominantly associated with the cell populations in heart-forming regions, somites, neural folds, notochord and the presumptive thyroid. In stark contrast, in the vitamin A-deficient quail embryo RARβ2 was not expressed in any of the above cell populations. We conclude that the expressions of RARβ and CRABP I are developmentally regulated. Additionally, the expression of RARβ2 during early embryogenesis is regulated by vitamin A status. We propose that RARβ2 plays an important role in the mechanism of action of retinoids in early avian development. The lack of expression of RARβ2 may be linked to abnormalities of the cardiovascular system.