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. 2017 Aug 28;37(18):e00145-17. doi: 10.1128/MCB.00145-17

FIG 5.

FIG 5

(A) Schematic representation of the DVL1 DEP domain truncation mutants used for the rescue experiments. (B) DVL KO HEK293 cells were transfected with the indicated DVL1 mutants and V5-FZD5 or HA-axin1 and stained by immunocytochemistry. (Top) DVL1 only; (middle) DVL1 (green) and FZD5 (red); (bottom) DVL1 (green) and axin1 (red). Bar, 7.5 μm. (C) Quantification of DVL1 localization after FZD5 cotransfection. The evaluation criteria used were the same as those described in the legend to Fig. 4B. None of the truncation mutants was recruited to the membrane by FZD5. (D) TopFlash reporter assay analysis of DVL1 mutants with the DEP domain truncation (n = 4). Only the DVL1(1–438) mutant showed a weak ability to rescue TCF/LEF-dependent transcription. (E) WB analysis of expression levels of individual mutants and their ability to rescue phosphorylation of S1490-LRP6 (n = 3). None of the mutants could rescue S1490-LRP6 phosphorylation. Analysis for statistically significant differences was performed by paired Student's t test (*, P < 0.05; **, P < 0.01).