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Fig. 7 | Genome Biology

Fig. 7

From: Pediatric glioma histone H3.3 K27M/G34R mutations drive abnormalities in PML nuclear bodies

Fig. 7

PML-NBs and arsenic trioxide treatment of IDH1 R132H mutated oligodendroglioma cells. A Immunostaining of ATRX (green) and PML (red) in WT and heterozygous IDH1 R132H mouse ES cells. Scale bar 2 µM. B Quantitation of PML-NBs per cell. Fifty nuclei (n = 50) were counted per cell line from three independent immunofluorescence experiments. Dots represent counts per cell. P-values were calculated using two-tailed Student’s t test (*P < 0.0001). C dSTORM quantitation of Feret diameter (size) of PML nuclear bodies in WT (n = 292), IDH1 R132H (n = 256) cells. 25th, median, and 75th percentiles are shown. P-values were calculated using a two-tailed Mann–Whitney U test (**P < 0.005). D Immunostaining of ATRX (green) and PML (red) in IDH1 WT (R132H KO) and BT237 IDH1 R132H patient-derived glioma cells. Scale bar 2 µM. E PML-NBs per cell in IDH1 KO and IDH1 R132H mutant cells. Dots represent counts per cell (n = 103). 25th, median, and 75th percentiles are shown. P-values were calculated using two-tailed Student’s t test (***P < 0.0001). Cell counts of F IDH1 WT (R132H KO) and G IDH1 R132H pediatric glioma cells treated with 1 µM of arsenic trioxide for 0, 4, and 8 days compared to untreated controls. Points and error bars represent the mean average and standard deviation of three independent experiments. P-values were calculated using two-tailed Student’s t test (*P < 0.005)

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