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植物配子发生过程中的DNA甲基化与表观遗传继承

DNA methylation and epigenetic inheritance during plant gametogenesis.

作者信息

Takeda Shin, Paszkowski Jerzy

机构信息

Laboratory of Plant Genetics, University of Geneva, Science III, Switzerland.

出版信息

Chromosoma. 2006 Feb;115(1):27-35. doi: 10.1007/s00412-005-0031-7. Epub 2005 Oct 26.

Abstract

In plants, newly acquired epigenetic states of transcriptional gene activity are readily transmitted to the progeny. This is in contrast to mammals, where only rare cases of transgenerational inheritance of new epigenetic traits have been reported (FASEB J 12:949-957, 1998; Nat Genet 23:314-318, 1999; Proc Natl Acad Sci U S A 100:2538-2543, 2003). Epigenetic inheritance in plants seems to rely on cytosine methylation maintained through meiosis and postmeiotic mitoses, giving rise to gametophytes. In particular, maintenance of CpG methylation ((m)CpG) appears to play a central role, guiding the distribution of other epigenetic signals such as histone H3 methylation and non-CpG DNA methylation. The evolutionarily conserved DNA methyltransferase MET1 is responsible for copying (m)CpG patterns through DNA replication in the gametophytic phase. The importance of gametophytic MET1 activity is illustrated by the phenotypes of met1 mutants that are severely compromised in the accuracy of epigenetic inheritance during gametogenesis. This includes elimination of imprinting at paternally silent loci such as FWA or MEDEA (MEA). The importance of DNA methylation in gametophytic imprinting has been reinforced by the discovery of DEMETER (DME), encoding putative DNA glycosylase involved in the removal of (m)C. DME opposes transcriptional silencing associated with imprinting activities of the MEA/FIE polycomb group complex.

摘要

在植物中,转录基因活性新获得的表观遗传状态很容易传递给后代。这与哺乳动物形成对比,在哺乳动物中,仅有罕见的新表观遗传性状跨代遗传的案例被报道(《美国实验生物学联合会会刊》12:949 - 957,1998年;《自然遗传学》23:314 - 318,1999年;《美国国家科学院院刊》100:2538 - 2543,2003年)。植物中的表观遗传遗传似乎依赖于通过减数分裂和减数分裂后有丝分裂维持的胞嘧啶甲基化,从而产生配子体。特别地,CpG甲基化((m)CpG)的维持似乎起着核心作用,引导其他表观遗传信号如组蛋白H3甲基化和非CpG DNA甲基化的分布。进化上保守的DNA甲基转移酶MET1负责在配子体阶段通过DNA复制复制(m)CpG模式。配子体MET1活性的重要性通过met1突变体的表型得以体现,这些突变体在配子发生过程中表观遗传遗传的准确性严重受损。这包括消除父本沉默位点如FWA或MEA(MEA)的印记。DNA甲基化在配子体印记中的重要性因DEMETER(DME)的发现而得到加强,DME编码参与去除(m)C的推定DNA糖基化酶。DME对抗与MEA/FIE多梳蛋白组复合体的印记活性相关的转录沉默。

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