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拟南芥DNA聚合酶ε招募多梳抑制复合物的组分以介导表观遗传基因沉默。

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

作者信息

Del Olmo Iván, López Juan A, Vázquez Jesús, Raynaud Cécile, Piñeiro Manuel, Jarillo José A

机构信息

Centro de Biotecnología y Genómica de Plantas (CBGP), UPM-INIA, Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria, Campus de Montegancedo, 28223 Madrid, Spain.

Proteomics Unit, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), 28029 Madrid, Spain.

出版信息

Nucleic Acids Res. 2016 Jul 8;44(12):5597-614. doi: 10.1093/nar/gkw156. Epub 2016 Mar 14.

Abstract

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.

摘要

拟南芥ESD7基因座编码参与DNA前导链合成的DNA聚合酶ε的催化亚基,对胚胎活力至关重要。亚效等位基因esd7-1是可存活的,但表现出许多多效性表型改变,包括开花时间加速。此外,DNA聚合酶ε参与开花整合基因FT和SOC1的表观遗传沉默,但所涉及的转录基因沉默机制的分子本质仍不清楚。在这里,我们揭示ESD7与PRC2的组分如CLF、EMF2和MSI1相互作用,并且ESD7中的突变导致FT和SOC1染色质中存在的H3K27me3标记水平降低。我们还证明ESD7 C末端区域的一个结构域介导与不同PRC2组分的结合,并且这种相互作用对于将PRC2正确募集到FT和SOC1染色质是必需的。我们揭示了DNA复制机制与PcG复合物在表观遗传转录沉默中的相互作用。这些观察结果为确保发育控制中关键位点的表观遗传密码被忠实地传递给真核细胞后代的机制提供了见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3312/4937302/899091d294f2/gkw156fig1.jpg

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