Fig. 6: Wnt-PCP loss alters Jnk-c-Jun signalling in biliary cells.

a Biliary organoids from Vangl2^WT mice or Vangl2^flox mice (following treatment with Cre lentivirus, known as Vangl2^ΔTM), immunostained for VANGL2 (red) membrane-bound E-cadherin (green), upper panels. White arrows denote co-immunofluorescence, whereas red arrows denote residual small Vangl2 puncta, not localised to the cell membrane. Lower panels represent the same conditions as described in (a), but stained for phosphorylated c-JUN^S73 (red) and E-cadherin, white. b Western blot of proteins from Vangl2^WT and Vangl2^ΔTM biliary organoids. c Relative mRNA expression Wnt-PCP target genes, Ctgf and Mmp7 normalised to the housekeeping gene Ppia from Vangl2^WT and Vangl2^ΔTM biliary organoids. d Immunofluorescent staining of tdTomato (red), phosphorylated Jnk^T183/Y185 or phosphorylated c-JUN^S73 (green) and DNA (blue) in mice where Vangl2 has been deleted specifically in biliary epithelial cell (Keratin-19-CreER^T::Vangl2^flox, following Cre activation known as Keratin-19-CreER^T::Vangl2^ΔTM). White arrows denote dual-positive cells and yellow arrows denote cells that are only tdTomato (red) positive. e mRNA expression of Ctgf and Mmp7 normalised to the housekeeping gene Ppia in bile ducts isolated from Keratin-19-CreER^T::Vangl2^ΔTM mice following DDC injury. f Histological quantification of CTGF protein in Keratin-19-CreER^T::Vangl2^ΔTM mice following DDC-induced bile duct injury. g Histological quantification of total fibrillar collagen (Picrosirius Red, PSR), Collagen-1 and h Desmin (fibroblasts) following DDC treatment of Keratin-19-CreER^T::Vangl2^ΔTM mice. Scale bar = 50 µm. Source data are provided as a Source Data file. In all graphs, a Student’s t test is used. Box–whisker plots represent min–max range of the data. In dot plots, data are presented as mean ± S.E.M. Each data point (N) represents an individual animal. In (c), each N represents an experimental replicate.