Fig. 6: β-Catenin GOF causes upregulation of β-III TUBULIN in TTR + ChPe cells.

(a–c) At E12.5, both control and Lmx1aCre::β-Catenin GOF ChP display a ribbon-like morphology and do not express hem markers Wnt2b and BLBP (a) but express Ttr mRNA and TTR protein (b). (c) Co-immunostaining for β-III TUBULIN and TTR identifies cells that display both markers in the β-Catenin GOF but not in the control ChPe. (a–c) Representative images are shown of sections taken from N = 3 brains (biologically independent replicates) examined over 2 independent experiments. Boxed regions (c) are shown at high magnification in the adjacent panels. (d–g) At E13.5, male Lmx1aCre::Ai9 control and Lmx1aCre::Ai9::β-Catenin GOF brains display Cre-driven Ai9-positive cells throughout the ChPe (d, f), In contrast, female control and β-Catenin GOF brains show mosaic Ai9 due to random X-inactivation (e, g). β-III TUBULIN is undetectable in the female control ChPe, but appears selectively in the Ai9+ patches in the female β-Catenin GOF ChPe (e, g). (h–k). In females, neither control Lmx1aCre::Ai9 ChPe cells (cells #1–4; h, i) nor non-Ai9 cells internal control cells in Lmx1aCre::Ai9::β-Catenin GOF ChPe (cells #5–8; j, k) display co-localization of β-III TUBULIN and TTR. These markers are both detected in Ai9-positive Lmx1aCre::Ai9::β-Catenin GOF ChPe cells (#9–12; l, m). (d–l), Representative images are shown of sections taken from N = 3 brains (biologically independent replicates) examined over 2 independent experiments. (i, k, m) Fluorescence intensity quantifications of cells #1–12 from (h, j, l). Boxed regions (e, g) are shown at high magnification in the panels (h, j, l) below. Scale bars: 10 μm (all high mag panels in c and all panels in h–l); 50 μm (all panels in a–e). Further information on replicates and reproducibility for this figure is mentioned in the “Statistics and Reproducibility” section of the Methods. Source data are provided as a Source Data file.