Retinoid receptors, which are members of the nuclear hormone receptor
superfamily, act as ligand-dependent transcription factors. They media
te the effects of retinoic acid primarily as heterodimers of retinoic
acid receptors (RARs) and retinoid X receptors (RXRs). To analyse thei
r function, xRXR beta synthetic mRNA was injected into Xenopus embryos
in combination with normal and mutated xRAR alpha transcripts. Two in
formative phenotypes are reported here. Firstly, over-expression of xR
XR beta with xRAR alpha results in the formation of ectopic primary ne
urons, Secondly, blocking retinoid signalling with a mutated xRAR alph
a results in a lack of primary neurons. These two phenotypes, from con
tra-acting manipulations, indicate a role for retinoid signalling duri
ng neurogenesis.