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. 2018 May 15;29(10):1178–1189. doi: 10.1091/mbc.E17-10-0600

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© 2018 Eguether et al. “ASCB®,” “The American Society for Cell Biology®,” and “Molecular Biology of the Cell®” are registered trademarks of The American Society for Cell Biology.

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FIGURE 3: — Ift27 and Lztfl1 mutant cells are defective in Gli2/3 expression and processing. (A–C) Immunoblots of Gli2 and Gli3 in wild-type, Ift27, Bbs2, and Lztfl1 knockout cells transfected or not with SmoM2. GAPDH is the loading control. Quantification of Gli2 (B), Gli3 full length (Gli3FL), and repressor form (Gli3R) (C) expression from three experiments normalized to untransfected cells expression. (D, E) Quantification of Gli2 (D), Gli3 full length (Gli3FL), and repressor form (Gli3R) (E) expression from three experiments normalized to wild-type cells expression. (F) Wild type, Ift27. (F) Pairs of control and SmoM2-transfected cells were lysed, immunoprecipitated with SuFu antibody, and analyzed by immunoblotting with Gli2 antibody to evaluate SuFu/Gli2 binding. (G) Pairs of control and SmoM2-transfected cells were lysed, immunoprecipitated with SuFu antibody and analyzed by immunoblotting with Gli3 antibody to evaluate SuFu/Gli3 binding. (H, I) Quantification of Gli2 (H) and Gli3 full-length (I) expression from three experiments normalized to untransfected cells expression. Graphs represent three technical replicates. Error bars are SD. Data were analyzed using one-way ANOVA followed with Tukey’s multiple comparison test.