The role of DNA methylation, nucleosome occupancy and histone modifications in paramutation
The role of DNA methylation, nucleosome occupancy and histone modifications in paramutation
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DOI：
10.1111/j.1365-313x.2010.04245.x
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发表时间：
2010-08-01
期刊：
影响因子：
7.2
通讯作者：
Stam, Maike
中科院分区：
文献类型：
--
作者：
Haring, Max;Bader, Rechien;Stam, Maike
P>副突变是等位基因之间表观遗传信息的转移，导致这些等位基因之一的表达发生可遗传的变化。组织特异性表达的玉米 (Zea mays) b1 基因座的副突变涉及低表达 B' 和高表达 B-I 等位基因。在同一个细胞核中结合，B' 遗传性地将 B-I 变为 B'。副突变和高 b1 表达需要位于 b1 编码区上游 100 kb 的七重复序列。表观遗传修饰在副突变中的作用目前尚不清楚。在这项研究中，我们表明 B' 七重复序列在所有分析的组织中都是 DNA 高甲基化的。重要的是，将 B' 和 B-I 组合在一个核中会导致植物发育早期 B-I 重复序列从头甲基化。这些发现表明七重复 DNA 甲基化在沉默 B' 状态的建立和维持中的作用。相反，核小体占据、H3 乙酰化以及 H3K9 和 H3K27 甲基化主要参与七重复的组织特异性调节。核小体耗竭和 H3 乙酰化在 B-1 七重复序列上受到组织特异性调节，并与 b1 表达的增强相关。 H3K9 和 H3K27 甲基化是组织特异性定位于 B' 七重复序列，并强化 B' 染色质沉默状态。在所有分析的组织中，B' 编码区都是 H3K27 二甲基化，表明在维持沉默的 B' 状态中发挥作用。总而言之，这些发现提供了对 b1 在染色质结构水平上的副突变和组织特异性调节的机制的深入了解。
P>Paramutation is the transfer of epigenetic information between alleles that leads to a heritable change in expression of one of these alleles. Paramutation at the tissue-specifically expressed maize (Zea mays) b1 locus involves the low-expressing B' and high-expressing B-I allele. Combined in the same nucleus, B' heritably changes B-I into B'. A hepta-repeat located 100-kb upstream of the b1 coding region is required for paramutation and for high b1 expression. The role of epigenetic modifications in paramutation is currently not well understood. In this study, we show that the B' hepta-repeat is DNA-hypermethylated in all tissues analyzed. Importantly, combining B' and B-I in one nucleus results in de novo methylation of the B-I repeats early in plant development. These findings indicate a role for hepta-repeat DNA methylation in the establishment and maintenance of the silenced B' state. In contrast, nucleosome occupancy, H3 acetylation, and H3K9 and H3K27 methylation are mainly involved in tissue-specific regulation of the hepta-repeat. Nucleosome depletion and H3 acetylation are tissue-specifically regulated at the B-I hepta-repeat and associated with enhancement of b1 expression. H3K9 and H3K27 methylation are tissue-specifically localized at the B' hepta-repeat and reinforce the silenced B' chromatin state. The B' coding region is H3K27 dimethylated in all tissues analyzed, indicating a role in the maintenance of the silenced B' state. Taken together, these findings provide insight into the mechanisms underlying paramutation and tissue-specific regulation of b1 at the level of chromatin structure.