Analysis of H3K79 methylation during reprogramming. Homo sapiens

Chromatin immunoprecipitation followed by Solexa sequencing for H3K27me3 and H3K79me2 in Fibroblasts, Embryonic stem cells, and fibroblast undergoing reprogramming Overall design: Inhibition of the histone 3 lysine 79 (H3K79) methyltransferase increases repgoramming efficiency and genome-wide analysis of H3K79me2 distribution revealed that fibroblast-specific genes associated with the epithelial to mesenchymal transition lose H3K79me2 in the initial phases of reprogramming. Dot1L inhibition facilitates the loss of this mark from genes that are fated to be repressed in the pluripotent state.

本数据集为针对成纤维细胞（Fibroblasts）、胚胎干细胞（Embryonic stem cells）以及正在进行重编程的成纤维细胞中的组蛋白H3第27位赖氨酸三甲基化（H3K27me3）与组蛋白H3第79位赖氨酸二甲基化（H3K79me2）的染色质免疫共沉淀结合Solexa测序数据。
实验设计：抑制组蛋白3赖氨酸79（H3K79）甲基转移酶可提升重编程效率；全基因组范围的H3K79me2分布分析显示，与上皮间质转化（epithelial to mesenchymal transition, EMT）相关的成纤维细胞特异性基因在重编程初始阶段会丢失H3K79me2修饰。Dot1L抑制可促进该修饰从多能状态下注定被沉默的基因上丢失。