All-trans-retinoic acid upregulates the expression of COUP-TFI in early-somite mouse embryos cultured in vitro.
Exposure of embryos to an excess of retinoic acid (RA) modifies the spatio-temporal pattern of expression of developmental genes. RA regulates the expression of target genes through binding of the retinoid nuclear receptors (RARs and RXRs), as heterodimers, to regulatory cis-acting elements. COUP-TF factors, which are able to dimerize with the RXRs and to compete with the retinoid receptors for their DNA binding sites, are suspected to modulate the retinoid signal transduction pathway. Therefore, COUP-TF factors may be involved in the regulation of the expression of developmental genes and/or in the modifications induced by an excess of RA in the expression of these genes. The aim of this work is to assess whether RA-induced modifications in the expression of Krox-20 and Hox genes correlate with alterations of the expression of COUP-TF genes. In addition to spatial modifications in the expression patterns of Krox-20 and Hox genes, we report here an upregulation of the expression level of COUP-TFI after RA exposure. However, this abnormality did not spatially overlap with the modifications observed in the expression of Krox-20 and Hox genes. These data suggest an involvement of COUP-TFI in the generation of RA-induced abnormalities, but do not support the hypothesis of an involvement of this factor in the regulation of the expression of Hox or Krox-20 genes.
Clotman
F
F
Center for Transgene Technology and Gene Therapy, Flanders Interuniversity Institute for Biotechnology, Leuven, Belgium.
Van Maele-Fabry
G
G
Picard
J J
JJ
D000818:Animals; D051838:COUP Transcription Factor I; D004268:DNA-Binding Proteins / Q000096:biosynthesis* / Q000378:metabolism; D051767:Early Growth Response Protein 2; D004622:Embryo, Mammalian / Q000187:drug effects* / Q000378:metabolism; D015870:Gene Expression / Q000187:drug effects*; D018398:Homeodomain Proteins / Q000378:metabolism; D017403:In Situ Hybridization; D066298:In Vitro Techniques; D051379:Mice; D011965:Receptors, Glucocorticoid / Q000378:metabolism; D014157:Transcription Factors / Q000096:biosynthesis* / Q000378:metabolism; D014212:Tretinoin / Q000494:pharmacology*
D051838:COUP Transcription Factor I; D004268:DNA-Binding Proteins; D051767:Early Growth Response Protein 2; C497327:Egr2 protein, mouse; C101121:HOXB1 homeodomain protein; D018398:Homeodomain Proteins; C490111:Hoxb2 protein, mouse; C497590:Nr2f1 protein, mouse; D011965:Receptors, Glucocorticoid; D014157:Transcription Factors; D014212:Tretinoin