Department of Pharmacology and Therapeutics, Faculty of Medicine, McGill University, Montreal, Quebec, Canada.
Nat Protoc. 2022 Dec;17(12):2840-2881. doi: 10.1038/s41596-022-00741-3. Epub 2022 Oct 7.
DNA methylation involves the enzymatic addition of a methyl group primarily to cytosine residues in DNA. This protocol describes how to produce complete and minimally confounded DNA demethylation of specific sites in the genome of cultured cells by clustered regularly interspaced short palindromic repeats (CRISPR)-dCas9 and without the involvement of an epigenetic-modifying enzyme, the purpose of which is the evaluation of the functional (i.e., gene expression or phenotypic) consequences of DNA demethylation of specific sites that have been previously implicated in particular pathological or physiological contexts. This protocol maximizes the ability of the easily reprogrammable CRISPR-dCas9 system to assess the impact of DNA methylation from a causal rather than correlational perspective: alternative protocols for CRISPR-dCas9-based site-specific DNA methylation or demethylation rely on the recruitment of epigenetic enzymes that exhibit additional nonspecific activities at both the targeted site and throughout the genome, confounding conclusions of causality of DNA methylation. Inhibition or loss of DNA methylation is accomplished by three consecutive lentiviral transductions. The first two lentiviruses establish stable expression of dCas9 and a guide RNA, which will physically obstruct either maintenance or de novo DNA methyltransferase activity at the guide RNA target site. A third lentivirus introduces Cre recombinase to delete the dCas9 transgene, which leads to loss of dCas9 from the target site, allowing transcription factors and/or the transcription machinery to interact with the demethylated target site. This protocol requires 3-8 months to complete owing to prolonged cell passaging times, but there is little hands-on time, and no specific skills beyond basic molecular biology techniques are necessary.
DNA 甲基化涉及酶促将甲基基团主要添加到 DNA 中的胞嘧啶残基上。本方案描述了如何通过成簇规律间隔短回文重复序列 (CRISPR)-dCas9 并在不涉及表观遗传修饰酶的情况下,对培养细胞基因组中的特定位点进行完整且最小干扰的 DNA 去甲基化,其目的是评估特定位点的 DNA 去甲基化的功能(即基因表达或表型)后果,这些特定位点先前与特定病理或生理背景有关。该方案最大限度地提高了易于重新编程的 CRISPR-dCas9 系统从因果而不是相关角度评估 DNA 甲基化影响的能力:基于 CRISPR-dCas9 的用于特定位点的 DNA 甲基化或去甲基化的替代方案依赖于招募表观遗传酶,这些酶在靶位点和整个基因组中都表现出额外的非特异性活性,从而混淆了 DNA 甲基化因果关系的结论。通过连续三次慢病毒转导来实现 DNA 去甲基化或抑制。前两个慢病毒建立 dCas9 和向导 RNA 的稳定表达,这将在向导 RNA 靶位点处物理阻止维持或从头 DNA 甲基转移酶活性。第三个慢病毒引入 Cre 重组酶以删除 dCas9 转基因,这导致 dCas9 从靶位点丢失,允许转录因子和/或转录机制与去甲基化靶位点相互作用。由于细胞传代时间延长,该方案需要 3-8 个月才能完成,但实际操作时间很少,并且除了基本的分子生物学技术之外,不需要特定的技能。