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表观遗传突变与 CHROMOMETHYLASE 3 诱导的从头 DNA 甲基化有关。

Epimutations are associated with CHROMOMETHYLASE 3-induced de novo DNA methylation.

机构信息

Department of Genetics, University of Georgia, Athens, United States.

Institute of Bioinformatics, University of Georgia, Athens, United States.

出版信息

Elife. 2019 Jul 29;8:e47891. doi: 10.7554/eLife.47891.

DOI:10.7554/eLife.47891
PMID:31356150
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6663294/
Abstract

In many plant species, a subset of transcribed genes are characterized by strictly CG-context DNA methylation, referred to as gene body methylation (gbM). The mechanisms that establish gbM are unclear, yet flowering plant species naturally without gbM lack the DNA methyltransferase, CMT3, which maintains CHG (H = A, C, or T) and not CG methylation at constitutive heterochromatin. Here, we identify the mechanistic basis for gbM establishment by expressing in a species naturally lacking expression reconstituted gbM through a progression of de novo CHG methylation on expressed genes, followed by the accumulation of CG methylation that could be inherited even following loss of the transgene. Thus, gbM likely originates from the simultaneous targeting of loci by pathways that promote euchromatin and heterochromatin, which primes genes for the formation of stably inherited epimutations in the form of CG DNA methylation.

摘要

在许多植物物种中,一组转录基因的特征是严格的 CG 上下文 DNA 甲基化,称为基因体甲基化(gbM)。建立 gbM 的机制尚不清楚,但天然缺乏 gbM 的开花植物物种缺乏维持组成型异染色质中 CHG(H = A、C 或 T)而非 CG 甲基化的 DNA 甲基转移酶 CMT3。在这里,我们通过在天然缺乏表达的物种中表达 ,鉴定了 gbM 建立的机制基础,通过在表达基因上进行从头 CHG 甲基化的逐步发展,重新构建了 gbM,随后是 CG 甲基化的积累,即使在失去 转基因后,这种甲基化也可以遗传。因此,gbM 可能源自促进常染色质和异染色质的途径同时靶向基因座,这为以 CG DNA 甲基化形式形成稳定遗传的表观突变奠定了基础。

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