Figure 6. TAZ/YAP activation drives an oncogenic growth program in Lats1/2-deficient SCs.

(A) Isolation of GFP⁺ reporter-expressing SC cells by FACS from dissociated control SNs and Lats1/2-deficient paraspinal or nerve-associated tumors.

(B) Heatmap shows differentially expressed genes in Lats1/2-deficient GFP⁺ SCs (n = 6 mice) compared with control GFP⁺ SCs (n = 3 mice).

(C) Volcano plot of transcriptome profiles between control GFP⁺ SCs and Lats1/2-deficient GFP⁺ SCs. Red and blue dots represent genes significantly upregulated and downregulated in Lats1/2-deficient GFP⁺ SCs (p < 0.02, FDR < 0.1), respectively.

(D) Heatmap shows changes of pathway activity between control GFP⁺ SCs (n = 3) and Lats1/2-deficient GFP⁺ SCs (n = 6) based on MSigDB gene sets. Expression signature scores are the means with linkage hierarchical clustering.

(E) GSEA analysis of Lats1/2-deficient GFP⁺ SCs (n = 6) and control GFP⁺ SCs (n = 3) for top differentially regulated gene sets.

(F) GSEA plots of Lats1/2-deficient GFP⁺ SCs (Lats1/2-deficient tumor) show upregulation of YAP conserved signature (left) and YAP activated signature (right).

(G) GSEA plots of Lats1/2-deficient GFP⁺ SCs show downregulation of axon ensheathment (left) and Egr2 targets (right) gene sets.

(H) ToppCluster analysis of upregulated gene sets in Lats1/2-deficient GFP⁺ SCs.

See also Figure S6.