PRC1 and Suv39h specify parental asymmetry at constitutive heterochromatin in early mouse embryos
PRC1 and Suv39h specify parental asymmetry at constitutive heterochromatin in early mouse embryos
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DOI：
10.1038/ng.99
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发表时间：
2008-04-01
期刊：
影响因子：
30.8
通讯作者：
Peters, Antoine H. F. M.
中科院分区：
文献类型：
--
作者：
Puschendorf, Mareike;Terranova, Remi;Peters, Antoine H. F. M.
在真核生物中，Suv39hH3K9三甲基转移酶是着丝粒周围异染色质形成和功能所必需的。然而，在小鼠植入前的早期胚胎中，父亲的着丝粒周围异染色质缺乏Suv39h介导的H3K9me3及其下游标记。在这里，我们展示了母亲提供的多梳抑制复合体1(PRC1)成分的Ezh2非依赖性靶向到父亲的异染色质。在Suv39h2母性缺陷受精卵中，Prc1还与缺乏H3K9me3的母体异染色质相关，从而揭示了抑制途径之间的等级关系。在Rnf2母系缺陷受精卵中，Prc1复合体被破坏，着丝粒周围主要卫星转录水平在父亲基因组中增加，但在母体基因组中不增加。我们的结论是，在早期胚胎中，Suv39h介导的H3K9me3是形成着丝粒异染色质的主要母体跨代信号。在没有该信号的情况下，PRC1充当默认的抑制备份机制。亲代表观遗传的不对称性，也在分裂染色体上观察到，在8细胞阶段结束时得到解决--同时伴随着卵裂球的极化--标志着母体向胚胎转变的结束。
In eukaryotes, Suv39h H3K9 trimethyltransferases are required for pericentric heterochromatin formation and function. In early mouse preimplantation embryos, however, paternal pericentric heterochromatin lacks Suv39h-mediated H3K9me3 and downstream marks. Here we demonstrate Ezh2-independent targeting of maternally provided polycomb repressive complex 1 (PRC1) components to paternal heterochromatin. In Suv39h2 maternally deficient zygotes, PRC1 also associates with maternal heterochromatin lacking H3K9me3, thereby revealing hierarchy between repressive pathways. In Rnf2 maternally deficient zygotes, the PRC1 complex is disrupted, and levels of pericentric major satellite transcripts are increased at the paternal but not the maternal genome. We conclude that in early embryos, Suv39h-mediated H3K9me3 constitutes the dominant maternal transgenerational signal for pericentric heterochromatin formation. In absence of this signal, PRC1 functions as the default repressive back-up mechanism. Parental epigenetic asymmetry, also observed along cleavage chromosomes, is resolved by the end of the 8-cell stage-concurrent with blastomere polarization-marking the end of the maternal-to-embryonic transition.