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Dev Biol. 2006 Nov 1;299(1):35-51. Epub 2006 Jul 4.

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

Author information

1
Laboratoire de Biologie du Développement, équipe Signalisation et Morphogenèse, UMR CNRS 7622, Université Paris VI, 9 quai Saint-Bernard, 75005 Paris, France.

Abstract

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.

PMID:
16979153
DOI:
10.1016/j.ydbio.2006.06.047
[Indexed for MEDLINE]
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