Arabidopsis DNA polymerase ϵ recruits components of Polycomb repressor complex to mediate epigenetic gene silencing.

Arabidopsis DNA polymerase ϵ recruits components of Polycomb repressor complex to mediate epigenetic gene silencing.
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DOI:
10.1093/nar/gkw156
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发表时间:
2016-07-08
影响因子:
14.9
通讯作者:
Jarillo JA
Jarillo JA
中科院分区:
生物学2区
文献类型:
--
作者:
Del Olmo I;López JA;Vázquez J;Raynaud C;Piñeiro M;Jarillo JA

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拟南芥ESD7位点编码DNA Pol柱的催化亚基,参与DNA前导链的合成,对胚胎存活至关重要。半形等位基因esd7-1是有活力的,但显示出许多多效表型改变,包括开花时间的加速。此外,Pol柱还参与了花整合子基因FT和SOC1的表观遗传沉默,但其转录基因沉默机制的分子性质尚不清楚。在这里,我们揭示了ESD7与PRC2的组分如CLF、EMF2和MSI1相互作用,并且ESD7的突变导致FT和SOC1染色质中存在的H3K27me3标记水平下降。我们还证明了ESD7 c端区域的一个结构域介导了与不同PRC2组分的结合,这种相互作用对于PRC2正确募集到FT和SOC1染色质是必要的。我们揭示了表观遗传转录沉默中DNA复制机制和PcG复合物之间存在相互作用。这些观察结果提供了一个深入了解的机制,确保在关键位点的表观遗传密码在发育控制是忠实地传递给真核细胞的后代。
Arabidopsis ESD7 locus encodes the catalytic subunit of the DNA Pol ϵ involved in the synthesis of the DNA leading strand and is essential for embryo viability. The hypomorphic allele esd7-1 is viable but displays a number of pleiotropic phenotypic alterations including an acceleration of flowering time. Furthermore, Pol ϵ is involved in the epigenetic silencing of the floral integrator genes FT and SOC1, but the molecular nature of the transcriptional gene silencing mechanisms involved remains elusive. Here we reveal that ESD7 interacts with components of the PRC2 such as CLF, EMF2 and MSI1, and that mutations in ESD7 cause a decrease in the levels of the H3K27me3 mark present in the chromatin of FT and SOC1. We also demonstrate that a domain of the C-terminal region of ESD7 mediates the binding to the different PRC2 components and this interaction is necessary for the proper recruitment of PRC2 to FT and SOC1 chromatin. We unveil the existence of interplay between the DNA replication machinery and the PcG complexes in epigenetic transcriptional silencing. These observations provide an insight into the mechanisms ensuring that the epigenetic code at pivotal loci in developmental control is faithfully transmitted to the progeny of eukaryotic cells.