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

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. Overall design: RNA-seq and ChIP-seq for three histone marks in cells and tumors from a mouse knock-in model of H3f3a K27M.

本研究构建了一款经工程化改造的小鼠敲入模型，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，进而生成带有或不带有K27M突变的表位标记（epitope-tagged）组蛋白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。
整体实验设计：针对该H3f3a K27M小鼠敲入模型的细胞及肿瘤样本，针对三种组蛋白修饰开展RNA测序（RNA-seq）与染色质免疫共沉淀测序（ChIP-seq）。