Involvement of MEM1 in DNA demethylation in Arabidopsis

Involvement of MEM1 in DNA demethylation in Arabidopsis
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MEM1 参与拟南芥 DNA 去甲基化

DOI:
10.1007/s11103-019-00949-0
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发表时间:
2020-01
影响因子:
5.1
通讯作者:
La Honggui
La Honggui
中科院分区:
生物学2区
文献类型:
--
作者:
Lu Yanke;Dai Jie;Yang Liu;La Yumei;Zhou Shaoxia;Qiang Sheng;Wang Qianqian;Tan Feng;Wu Yufeng;Kong Weiwen;La Honggui

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MEM 1参与ROS 1介导的DNA去甲基化途径,并与ROS 3一样抵消RdDM途径的影响,MEM 1突变导致拟南芥基因组中出现大量的高DMRs。在高等植物中,DNA甲基化在沉默转录基因和转座因子(TEs)中起重要作用。沉默恢复因子1(ROS 1)介导的主动DNA去甲基化能够拮抗RNA介导的DNA甲基化(RdDM)途径引起的DNA甲基化作用,对维持DNA甲基化水平具有重要作用。本研究利用Chop-PCR方法从T-DNA插入突变体群体中筛选出一个甲基化水平升高的突变体,命名为mem 1(methylation elevated mutant 1)。MEM 1具有一个Zf-C3 HC结构域,定位于细胞核中,并且在子叶中高度表达。全基因组亚硫酸氢盐测序数据显示,MEM 1的敲除突变导致4519个CG、1793个CHG和12739个CHH超DMR(对于差异甲基化区域)。进一步分析表明,mem 1 - 1与3个突变体(ros 1 -4、rdd和ros 3 -2)之间分别存在2751、2216和2042个重叠的CG hyper-DMR,与3个突变体(ros 1 -4、rdd和ros 3 -2)之间分别存在797、2514和6766个重叠的CHH hyper-DMR; mem 1 nrpd 1 -3和mem 1 rdm 1双突变体在4个测试位点上显示几乎完全或部分的超甲基化缺失,这表明MEM 1在抵消过度的DNA甲基化方面具有与DNA糖基化酶/裂解酶类似的功能,MEM 1作为沉默抑制因子3(ROS 3)在消除RdDM途径引起的CHH甲基化中起重要作用。总之,这些数据表明MEM 1参与ROS 1介导的DNA去甲基化途径以及MEM 1和ROS 3之间的功能连接。
MEM1 participates in ROS1-mediated DNA demethylation pathway, and acts functionally as ROS3 to counteract the effects of RdDM pathway.mem1mutation leads to large numbers of hyper-DMRs inArabidopsisgenome. In higher plants, DNA methylation performs important functions in silencing transcribed genes and transposable elements (TEs). Active DNA demethylation mediated by REPRESSOR OF SILENCING 1 (ROS1) is able to antagonize the action of DNA methylation caused by RNA-directed DNA methylation (RdDM) pathway, which plays critical roles in keeping DNA methylation at a proper level. In this study, a new mutant named mem1 (for methylation elevated mutant 1) was isolated from a genetic screen of T-DNA insertional mutant population for lines with elevated DNA methylation at a particular locus through Chop-PCR method. MEM1 possesses a Zf-C3HC domain, and is localized in nucleus as well as highly expressed in cotyledons. Whole-genome bisulfite sequencing data showed that knockout mutation of MEM1 leads to 4519 CG, 1793 CHG and 12739 CHH hyper-DMRs (for differentially methylated regions). Further analysis indicated that there are 2751, 2216 and 2042 overlapped CG hyper-DMRs between mem1-1and three mutants, i.e. ros1-4, rdd and ros3-2, respectively; 797, 2514, and 6766 overlapped CHH hyper-DMRs were observed between mem1-1 and three such mutants, respectively; mem1 nrpd1-3 and mem1 rdm1 double mutants showed nearly complete or partial loss of hypermethylation at 4 tested loci, suggesting that MEM1 performs similar functions as DNA glycosylase/lyases in counteracting excessive DNA methylation, and MEM1 plays important roles as REPRESSOR OF SILENCING 3 (ROS3) in erasing CHH methylation caused by the RdDM pathway. Together, these data demonstrate the involvement of MEM1 in ROS1-mediated DNA demethylation pathway and functional connections between MEM1 and ROS3.
DOI: 10.1371/journal.pgen.1004905
发表时间: 2015-01
期刊: PLoS genetics
影响因子: 4.5
作者:
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发表时间: 2012-02-10
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