Extended Data Figure 1: Mutational data in human MPNSTs and further biological analysis of SUZ12 loss.

a, Schematic overview of the deletions in the NF1, SUZ12 and EED regions observed in human MPNSTs (green, germline deletion; red, somatic deletion; yellow, duplication). b, List of the amino-acid changes or deletions found in SUZ12 and EED in human MPNSTs. c, Schematic representation of the location of SUZ12 and EED mutations (red, truncating mutation; green, missense mutation with amino-acid change noted). d, Immunoblots of lysates from primary human MPNSTs. Tumours with homozygous inactivating mutations in one of the PRC2 components (SUZ12 or EED) show complete loss of H3K27Me3. *Homozygous inactivation of EED. e, Immunoblots comparing NF1, SUZ12 and H3K27me3 expression of four human MPNST cell lines. *Cell line derived from an MPNST of a patient with an NF1 microdeletion. The human GBM cell lines A172 and U251 were used as a control. Corresponding NF1 mutations are reported in Extended Data Table 1 (S462, L2; 90-8TL, L3) and elsewhere in these NF1-deficient lines. p53 mutations, when known, are denoted and reported elsewhere²⁰. f, Proliferation curves used to derive bar graphs shown in Fig. 1d (red, LacZ control; green, SUZ12 reconstituted). g, Relative proliferation of several SUZ12 WT cell lines: colon (RKO, colo741, HCT-116) or GBM (T98G), after introduction of a control or SUZ12 lentivirus. None of these cell lines exhibited a significant decrease in proliferation under normal growth conditions or cell death in limiting growth factors, in contrast to SUZ12-deficient cells shown in Fig. 1d. h, Effects of shSUZ12 (S1) on colony formation (top) and SUZ12 expression (bottom) in A172 GBM cells, which are NF1 WT (see Extended Data Fig. 1e). i, Effects of shSUZ12 (S1) on SUZ12 expression and colony formation in WM3526 melanoma cells, which are NF1 WT. Error bars, s.d. (n = 3, biological replicates).