Fig. 6: H3K4me3 regulates transcription of cholesterol biosynthesis genes in glioblastoma.
From: Histone methyltransferase PRDM9 promotes survival of drug-tolerant persister cells in glioblastoma
a Genome wide H3K4me3 ChIPseq signal intensity (RPGC) (± 3 kb from transcription start/end site) in CMPD1 (10 µM, 3 days) treated RKI1 cells transduced with NTC sgRNA (NTC) or PRDM9 sgRNA (PRDM9 KO). b Combined intensity (RPGC) of H3K4me3 peaks aligning with a PRDM9 motif in CMPD1 (10 µM, 3 days) treated RKI1 cells transduced with NTC sgRNA (NTC) or PRDM9 sgRNA (PRDM9 KO). c Individual genome track of H3K4me3 intensity (RPGC) at an intergenic region aligning with PRDM9 motif (blue lines) in CMPD1 (10 µM, 3 days) treated RKI1 cells transduced with NTC sgRNA (NTC) or PRDM9 sgRNA (PRDM9 KO). d H3K4me3 genome tracks for cholesterol biosynthesis genes in CMPD1 (10 µM, 3 days) treated RKI1 cells transduced with NTC sgRNA (NTC) or PRDM9 sgRNA (PRDM9 KO). e Combined intensity (RPKM) of H3K4me3 peaks aligning with a PRDM9 motif in glioblastoma patient AK124 and AK231 (GSE121723)39. f H3K4me3 and H3K36me3 genome tracks at intergenic regions aligning with a PRDM9 motif in glioblastoma patients AK124 and AK231 (GSE121723)39. g H3K4me3 genome tracks for cholesterol biosynthesis genes in glioblastoma patients AK124 and AK231 (GSE121723)39. h Pearson’s correlation showing relationship between H3K4me3 peak widths and mRNA expression for DHCR7 and DHCR24 in n = 19 glioblastoma patients (GSE121723)39. Source data are provided as a Source Data file.
