Fig. 6: ARID1A directly binds YAP/TAZ and suppresses its activity.

A Heatmap showing relative expression (z-score) of known YAP-TEAD cardiac target genes in P7 Arid1a cKO and control hearts. B Relative expression (Fold change vs Control) of YAP (P = 0.6700), Taz (P = 0.2239), and Tead1 (P = 0.8537) in P7 Arid1a cKO (n = 4) and control hearts (n = 5) as determined by qPCR (two-tailed Student’s t-test). C Western blot analysis of total YAP and phosphorylated YAP (pYAP) in P7 control and Arid1a cKO hearts. Quantification indicates no difference in YAP (P = 0.6700) or pYAP (P = 0.2038) expression between control and Arid1a cKO hearts (n = 4; two-tailed Student’s t-test). Molecular weight marker (kDa) is shown at the right. D Relative expression of known YAP target genes Ccn1 (P = 0.0295), Ctgf (P = 0.0111), Sytl2 (P < 0.0001), and Igf1r (P = 0.0876) in Arid1a cKO (n = 4) and control hearts (n = 4–5) as determined by qPCR (*P < 0.05; ***P < 0.001, ****P < 0.0001, two-tailed Student’s t-test). E Representative example of 3 independent immunoprecipitations (IP) of FLAG-YAP and ARID1A in H10 cells, showing specific co-precipitation of ARID1A with YAP. Molecular weight marker (kDa) is shown at the right. F Luciferase assay with 8xGTIIC-luciferase YAP-TEAD reporter construct in H10 cells (Fold change versus siScr in GFP condition). Co-transfection of siRNA against Arid1a significantly induces reporter expression in the presence of YAP (P = 0.0028). pCDNA-GFP was used as a control vector. (**, P < 0.01. two-way ANOVA with Sidak’s multiple comparison test; n = 4 independent experiments). Bar graphs show mean with standard error of the mean. Source data are provided as a Source Data file.