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. 2022 Feb 1;13:604. doi: 10.1038/s41467-022-28198-8

Fig. 2. Expression of human PPM1Dtr potentiates DMG formation in vivo and requires the PPM1D phosphatase domain.

Fig. 2

A Plot showing ranked list of genes based on their expression Z-score in Ppm1d gRNA IUE DMG (n = 3 tumors). Top genes with expression Z-score > 15 are depicted. B Venn diagram showing highly expressed genes (Z-score > 2) in Ppm1d gRNA IUE DMG (n = 3), PPM1D-mutant human DMGs (n = 7), and the overlap between two datasets. Total number of genes analyzed in both datasets is shown outside the box. P < 6.27e−100 calculated using hypergeometric distribution. C Kaplan–Meier survival curves for control (n = 19), PPM1Dtr (n = 20), and PPM1Dtr-D314A (n = 10) IUE DMG mouse models. P = 0.002 between control vs. PPM1Dtr conditions calculated using log-rank Mantel–Cox test. D Brightfield and GFP images of control, PPM1Dtr, and PPM1Dtr-D314A IUE DMGs showing GFP-positive tumor regions, and H&E-stained images depicting high-grade glioma histology. Scale bar denotes 2.5 mm (brightfield and GFP) and 50 μm (H&E). Similar staining was performed in a minimum of three independent samples. E Control, PPM1Dtr, and PPM1Dtr-D314A IUE DMG sections stained with Olig2, Gfap, or Ki67. Scale bar denotes 50 μm. F Quantification of the percentage of Ki67-positive cells in Control (n = 9), PPM1Dtr (n = 8), and PPM1Dtr-D314A (n = 6) IUE DMG models. Data presented as mean ± SEM. P < 0.0001 for both control vs PPM1Dtr and PPM1Dtr vs PPM1Dtr-D314A conditions calculated using two-tailed t-test. Source data are provided as a Source Data file.