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Article Dans Une Revue Developmental Biology Année : 2006

Retinoic acid signalling is required for specification of pronephric cell fate.

Jérôme Cartry
  • Fonction : Auteur
Massimo Nichane
  • Fonction : Auteur
Vanessa Ribes
Alexandre Colas
  • Fonction : Auteur
Jean-Francois Riou
  • Fonction : Auteur
  • PersonId : 1189654
  • IdHAL : 509757
Tomas Pieler
  • Fonction : Auteur
Eric J Bellefroid
  • Fonction : Auteur
Muriel Umbhauer

Résumé

The mechanisms by which a subset of mesodermal cells are committed to a nephrogenic fate are largely unknown. In this study, we have investigated the role of retinoic acid (RA) signalling in this process using Xenopus laevis as a model system and Raldh2 knockout mice. Pronephros formation in Xenopus embryo is severely impaired when RA signalling is inhibited either through expression of a dominant-negative RA receptor, or by expressing the RA-catabolizing enzyme XCyp26 or through treatment with chemical inhibitors. Conversely, ectopic RA signalling expands the size of the pronephros. Using a transplantation assay that inhibits RA signalling specifically in pronephric precursors, we demonstrate that this signalling is required within this cell population. Timed antagonist treatments show that RA signalling is required during gastrulation for expression of Xlim-1 and XPax-8 in pronephric precursors. Moreover, experiments conducted with a protein synthesis inhibitor indicate that RA may directly regulate Xlim-1. Raldh2 knockout mouse embryos fail to initiate the expression of early kidney-specific genes, suggesting that implication of RA signalling in the early steps of kidney formation is evolutionary conserved in vertebrates.

Dates et versions

hal-00187854 , version 1 (15-11-2007)

Identifiants

Citer

Jérôme Cartry, Massimo Nichane, Vanessa Ribes, Alexandre Colas, Jean-Francois Riou, et al.. Retinoic acid signalling is required for specification of pronephric cell fate.. Developmental Biology, 2006, 299 (1), pp.35-51. ⟨10.1016/j.ydbio.2006.06.047⟩. ⟨hal-00187854⟩
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