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XB-ART-34427
Dev Biol November 1, 2006; 299 (1): 35-51.

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

Cartry J , Nichane M , Ribes V , Colas A , Riou JF , Pieler T , Dollé P , Bellefroid EJ , Umbhauer M .


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.

PubMed ID: 16979153
Article link: Dev Biol

Genes referenced: aldh1a2 atr cyp26a1 gal.2 lhx1 odc1 pax2 pax8 rab40b rara rarg rgn wt1


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