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. 2020 Aug 1;34(15-16):1051–1064. doi: 10.1101/gad.338681.120

Figure 5.

Figure 5.

Genetic disruption of YAP1–TEAD binding ablates tumor forming ability of YAP1 fusions. (A) TEAD1 IHC stainings of intracranial RCAS tumors in N/tv-a Cdkn2a-null mice. Scale bar, 25 µm. (B) YAP activity of S94A mutant YAP1 fusions (n = 3). (C) Combined knockdown of TEAD1–4 leads to reduced YAP activity of YAP1 fusions (n = 3). (D) PCA plot of S94A-YM and S94A-YF RNA-seq samples. (E–G) Symptom-free survival of N/tv-a Cdkn2a-null mice after intracranial expression of S94A mutant versions of YF (E), YS (F), or YT (G). (H) Tumor sizes after intracranial injection of murine neural stem cells expressing either unmutated or S94A mutant YM (n = 3 each). Error bars show SD. Analysis was done using two-tailed t-test (B,H), ordinary one-way ANOVA (C), and log rank (Mantel-Cox) test (E–G). (***) P < 0.001; (****) P < 0.0001.