Epigenetic changes in human DIPG cells with histone H3K27M mutations [ATAC-seq]. Epigenetic changes in human DIPG cells with histone H3K27M mutations [ATAC-seq]

We assessed changes in chromatin accessibility in H3.3K27M DIPG cell lines on knockdown of metabolic enzymes including HK2, GDH and IDH1 Overall design: Hexokinase-2 (HK2), Glutamate dehydrogenase (GLUD1) or insocitrate dehydrogenase (IDH1) were knocked down in H3.3K27M HSJD-DIPG007 cells. Genomic changes in chromatin accessibility were assessed between each shRNA and non-targeted NT controls.

本研究评估了H3.3K27M突变型弥漫内生型桥脑胶质瘤（Diffuse Intrinsic Pontine Glioma, DIPG）细胞系在敲低包括己糖激酶2（HK2）、谷氨酸脱氢酶（GDH，即GLUD1）、异柠檬酸脱氢酶1（IDH1）在内的代谢酶后，其染色质可及性（chromatin accessibility）的变化。
实验设计：在H3.3K27M HSJD-DIPG007细胞中分别敲低己糖激酶2（HK2）、谷氨酸脱氢酶（GLUD1）与异柠檬酸脱氢酶1（IDH1），并通过对比每一组短发夹RNA（short hairpin RNA, shRNA）实验组与非靶向NT（non-targeted）对照样本，评估染色质可及性的基因组水平变化。