Han Li, Lee Dong-Hoon, Szabó Piroska E
Division of Molecular Biology, Beckman Research Institute of the City of Hope, 1450 East Duarte Rd., Duarte, CA 91010-3011, USA.
Mol Cell Biol. 2008 Feb;28(3):1124-35. doi: 10.1128/MCB.01361-07. Epub 2007 Nov 26.
A paternally methylated imprinting control region (ICR) directs allele-specific expression of the imprinted H19 and Igf2 genes. CTCF protein binding in the ICR is required in the maternal chromosome for insulating Igf2 from the shared enhancers, initiation of the H19 promoter transcription, maintaining DNA hypomethylation, and chromosome loop formation. Using novel quantitative allele-specific chromatin immunoprecipitation-single-nucleotide primer extension assays, we measured the chromatin composition along the H19/Igf2 imprinted domain in cells with engineered mutations at the four ICR-CTCF binding sites. Abolishing CTCF binding in the ICR reduced normally maternal allele-specific H3K9 acetylation and H3K4 methylation at the H19 ICR and promoter/gene body and maternal allele-specific H3K27 trimethylation at the Igf2 P2 promoter and Igf2 differentially methylated regions (DMRs). Paternal H3K27 trimethylation and macroH2A1 became biallelic in the mutant cells at the H19 promoter while paternal H3K9 acetylation and H3K4 methylation became biallelic at the Igf2 DMRs. We provide evidence that CTCF is the single major organizer of allele-specific chromatin composition in this domain. This finding has important implications: (i) for mechanisms of insulation since CTCF regulates chromatin at a distance, involving repression by H3K27 trimethylation at the Igf2 locus independently of repression by DNA hypermethylation; and (ii) for mechanisms of genomic imprinting since point mutations of CTCF binding sites cause domain-wide "paternalization" of the maternal allele's chromatin composition.
父源甲基化的印记控制区域(ICR)指导印记基因H19和Igf2的等位基因特异性表达。母源染色体上ICR中的CTCF蛋白结合对于将Igf2与共享增强子隔离、启动H19启动子转录、维持DNA低甲基化以及形成染色体环是必需的。我们使用新型定量等位基因特异性染色质免疫沉淀-单核苷酸引物延伸分析,在四个ICR-CTCF结合位点发生工程突变的细胞中测量了H19/Igf2印记区域的染色质组成。消除ICR中的CTCF结合会降低H19 ICR和启动子/基因体处正常母源等位基因特异性的H3K9乙酰化和H3K4甲基化,以及Igf2 P_2启动子和Igf2差异甲基化区域(DMR)处母源等位基因特异性的H3K27三甲基化。在H19启动子处,父源H3K27三甲基化和macroH2A1在突变细胞中变为双等位基因,而在Igf2 DMR处,父源H3K9乙酰化和H3K4甲基化变为双等位基因。我们提供的证据表明,CTCF是该区域等位基因特异性染色质组成的单一主要组织者。这一发现具有重要意义:(i)对于绝缘机制而言,因为CTCF在远距离调节染色质,涉及Igf2基因座处H3K27三甲基化介导的抑制,独立于DNA高甲基化介导的抑制;(ii)对于基因组印记机制而言,因为CTCF结合位点的点突变会导致母源等位基因染色质组成在全区域的“父源化”。