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. 2008 Nov 3;183(3):377–384. doi: 10.1083/jcb.200808137

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© 2008 Jonassen et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jcb.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 5. — Deletion of Ift20 alters canonical Wnt signaling. (A) β-catenin staining of control (top rows) and experimental (bottom rows) kidneys at p10 and p33. Arrows indicate collecting ducts in controls and dilated or cystic ducts in experimental mice. Images are maximum projections of five confocal z images taken 0.5 μm apart (2 μm total). Control and experimental images at each of the time points were taken under identical conditions and manipulated uniformly, but the conditions were not the same at p10 and p33. Bar, 10 μm. (B) Western blot analysis of β-catenin. Control (Con) and experimental (Exp) kidneys were separated into cytosol and nuclear fractions and analyzed by Western blots with antibodies to β-catenin and dephosphorylated (active) β-catenin. RelB and GAPDH were used as loading controls. “1” and “2” represent different animals. (C) qPCR analysis of nine genes in experimental (closed bars) and control (open bars) kidneys at selected postnatal times. Gene expression data are normalized to GAPDH expression. Bars indicate mean ± SEM of 5–11 mice in each treatment and age group, plotted on logarithmic scales. *, P < 0.05; **, P < 0.01 (unpaired t tests).