Spontaneous DIPG Modeling Reveals Novel H3.3 K27M-Mediated Oncogenic Mechanisms Acting Through Epigenetic Effects

A mouse knock-in model engineered for Cre recombinase-activated expression of the endogenous mouse H3f3a allele generating an epitope-tagged H3.3 equipped with or without a K27M mutation to investigate H3.3 K27M effects on brain cell and tumor growth, gene expression and epigenetics. These samples are matched with H3K27me3 ChIPseq and RNAseq in GSE108364. Overall design: ChIP-seq for FLAG and H3K4me3 in neural stem cells from a mouse knock in model of H3f3a K27M (samples also appear in SuperSeries GSE108364).

本数据集基于经工程化改造的敲入小鼠模型，该模型可通过Cre重组酶（Cre recombinase）激活内源性小鼠H3f3a等位基因的表达，生成携带或不携带K27M突变的表位标记H3.3，用于探究H3.3 K27M突变对脑细胞与肿瘤生长、基因表达及表观遗传学的影响。本数据集的样本与GSE108364数据集中的H3K27me3染色质免疫共沉淀测序（ChIP-seq）及RNA测序（RNA-seq）数据相匹配。整体实验设计如下：针对H3f3a K27M敲入小鼠模型的神经干细胞，开展FLAG与H3K4me3的染色质免疫共沉淀测序，该部分样本同时收录于超级系列数据集GSE108364中。