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. 2008 Dec 26;4(12):e1000316. doi: 10.1371/journal.pgen.1000316

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Grote et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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(A, B) In situ hybridizations with a Gata3 cRNA probe reveal a strong downregulation of Gata3 expression in the nephric duct of E11.5 Ctnnb1^ND−/− embryos. (C, D) Likewise, in situ hybridizations with a Ret probe show a strong decrease of Ret expression in Ctnnb1-deficient nephric ducts. (E, F) Adjacent sections stained for the β-catenin transcriptional target Axin2, confirm loss of β-catenin signaling in Ctnnb1^ND−/− embryos. (G,H) Phosphorylated β-catenin levels are not significantly perturbed in Gata3^ND−/− embryos. E-cadherin was used as a nephric duct marker. (I–L) In situ hybridizations for Axin2 (I, J) and Daple (K, L) show a normal β-catenin signaling response in Gata3^ND−/− nephric ducts.