Retinoic acid prevents accumulation of a mesoderm-specific mRNA in the amphibian embryo

Our greatest progress in understanding mechanisms of germ layer specification in vertebrates has come from studies of mesoderm induction in amphibian embryos. A key early observation was that transcriptional activation of the muscle actin gene and accumulation of its mRNA can be used as molecular markers of mesoderm induction. Recent studies of putative amphibian morphogens have shown that exposure to all-trans retinoic acid (RA) can perturb both neural and mesodermal patterning in the Xenopus embryo, and that RA can, under certain conditions, induce the synthesis of mRNA for a gene whose product is able to influence the patterning of the embryo. To characterize further the mechanism of mesoderm induction, the effect of RA exposure on the transcriptional properties of the muscle actin gene has been investigated. Interestingly, prior exposure of embryos to RA appears to inhibit accumulation, rather than initial activation, of the mesoderm-specific muscle actin transcript. This effect is concentration-dependent and is not observed with the ubiquitously expressed genes for cytoskeletal actin and translation elongation factor 1 alpha, nor with a neural-specific beta-tubulin gene. Thus, the molecular mechanism of mesoderm induction may include, in addition to transcriptional activation of specific genes, processes involved in maintenance of mRNA accumulation for those gene products.