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EDM2 突变选择性地影响转座子的沉默状态,并诱导植物发育可塑性。

Mutations in EDM2 selectively affect silencing states of transposons and induce plant developmental plasticity.

机构信息

Institute for Integrative Genome Biology, Center for Plant Cell Biology, Department of Botany and Plant Sciences, University of California at Riverside, Riverside, CA 92521, USA.

出版信息

Sci Rep. 2013;3:1701. doi: 10.1038/srep01701.

DOI:10.1038/srep01701
PMID:23609044
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3632883/
Abstract

We previously reported on the A. thaliana gene EDM2, which is required for several developmental processes and race-specific immunity. Although EDM2 encodes a nuclear protein with features commonly observed in epigenetic factors, its role in chromatin silencing remains unknown. Here we demonstrate that silencing states of several transposons in edm2 mutants are altered. Levels of their transcripts anti-correlate with those of the repressive epigenetic marks H3K27me1, H3K9me2, and DNA-methylation at CHG sites. In addition, double mutant analysis revealed epistasis between EDM2 and the major histone H3K9-methyltransferase gene KRYPTONITE/SUVH4 in the control of H3K9me2 and CHG methylation. Moreover, we found that the expressivity of several mutant edm2 phenotypes exhibits stochastic variation reminiscent of mutants of known epigenetic modifiers. We propose that EDM2 affects the expression of transposons and developmentally important genes by modulating levels of repressive chromatin marks in a locus dependent manner.

摘要

我们之前曾报道过拟南芥基因 EDM2,它在几个发育过程和种特异性免疫中是必需的。尽管 EDM2 编码一种具有表观遗传因子常见特征的核蛋白,但它在染色质沉默中的作用尚不清楚。在这里,我们证明了 edm2 突变体中几种转座子的沉默状态发生了改变。它们的转录本水平与抑制性表观遗传标记 H3K27me1、H3K9me2 和 CHG 位点的 DNA 甲基化呈反相关。此外,双突变体分析显示,EDM2 与主要的组蛋白 H3K9 甲基转移酶基因 KRYPTONITE/SUVH4 之间存在上位性,共同控制 H3K9me2 和 CHG 甲基化。此外,我们发现,几个突变 edm2 表型的表现型具有类似于已知表观遗传修饰因子突变体的随机变异。我们提出,EDM2 通过在依赖于位置的方式下调节抑制性染色质标记的水平,影响转座子和发育重要基因的表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3699/3632883/917ad1a4fac0/srep01701-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3699/3632883/8d82a464641a/srep01701-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3699/3632883/ae202706a935/srep01701-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3699/3632883/31c0e00109db/srep01701-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3699/3632883/e1d5d0a1f988/srep01701-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3699/3632883/dc8a40c3d994/srep01701-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3699/3632883/917ad1a4fac0/srep01701-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3699/3632883/8d82a464641a/srep01701-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3699/3632883/ae202706a935/srep01701-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3699/3632883/31c0e00109db/srep01701-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3699/3632883/e1d5d0a1f988/srep01701-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3699/3632883/dc8a40c3d994/srep01701-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3699/3632883/917ad1a4fac0/srep01701-f6.jpg

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