Dynamic replacement of histone H3 variants reprograms epigenetic marks in early mouse embryos.
Dynamic replacement of histone H3 variants reprograms epigenetic marks in early mouse embryos.
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DOI：
10.1371/journal.pgen.1002279
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发表时间：
2011-10
期刊：
影响因子：
4.5
通讯作者：
Aoki F
中科院分区：
文献类型：
--
作者：
Akiyama T;Suzuki O;Matsuda J;Aoki F
受精后，基因表达的重编程是胚胎发育所必需的。这一步的标志是DNA去甲基化和组蛋白变异组成的变化。然而，引起这些变化的分子机制及其对组蛋白修饰的影响知之甚少。我们检测了小鼠受精后DNA复制依赖性组蛋白H3.1和H3.2变体以及DNA复制非依赖性组蛋白H3.3变体的全球沉积。我们发现，H3.3，一个基因活性的共色标记，从母体基因组中瞬间消失，表明H3.3携带的卵母细胞特异性修饰被擦除。受精后，H3.2被纳入转录沉默的异染色质中，而H3.1和H3.3分别占据异常的异染色质和常染色质位置。在两细胞期后，H3.1和H3.3变异体恢复其在异染色质和常染色质上各自的位置。通过敲低组蛋白伴侣蛋白caf1来阻止H3.1和H3.2的掺入，会导致H3.3沉积的相互增加，并损害异染色质的形成。我们认为不同H3变体的沉积影响染色质的功能组织。综上所述，这些发现表明，在表观遗传重编程过程中，H3变异沉积的动态变化对染色质重组至关重要。组蛋白在染色质结构和基因表达调控中发挥着重要作用。组蛋白H3非着丝粒变异（H3.1、H3.2和H3.3）的功能尚未完全了解。哺乳动物特异性H3.1的沉积模式和作用尚不清楚。我们在这里表明，这三种变体的核沉积在受精后和胚胎着床前发育过程中发生动态变化，在此过程中发生基因组重编程。激活基因标记H3.3在受精后很快从雌性原核中移除，表明分化卵母细胞中H3.3携带的表观遗传标记被删除。这一过程可能参与早期胚胎全能性的产生。在植入前晚期，H3.1似乎阻止了H3.3在非活性染色质区域的沉积。H3变异体沉积之间的相互作用可能参与了染色质的功能组织。总之，我们的研究结果表明，组蛋白变体的动态替换在基因组重塑中起着重要作用。
Upon fertilization, reprogramming of gene expression is required for embryo development. This step is marked by DNA demethylation and changes in histone variant composition. However, little is known about the molecular mechanisms causing these changes and their impact on histone modifications. We examined the global deposition of the DNA replication-dependent histone H3.1 and H3.2 variants and the DNA replication-independent H3.3 variant after fertilization in mice. We showed that H3.3, a euchromatic marker of gene activity, transiently disappears from the maternal genome, suggesting erasure of the oocyte-specific modifications carried by H3.3. After fertilization, H3.2 is incorporated into the transcriptionally silent heterochromatin, whereas H3.1 and H3.3 occupy unusual heterochromatic and euchromatin locations, respectively. After the two-cell stage, H3.1 and H3.3 variants resume their usual respective locations on heterochromatin and euchromatin. Preventing the incorporation of H3.1 and H3.2 by knockdown of the histone chaperone CAF-1 induces a reciprocal increase in H3.3 deposition and impairs heterochromatin formation. We propose that the deposition of different H3 variants influences the functional organization of chromatin. Taken together, these findings suggest that dynamic changes in the deposition of H3 variants are critical for chromatin reorganization during epigenetic reprogramming. Histones play essential roles in the regulation of chromatin structure and gene expression. The functions of histone H3 non-centromeric variants (H3.1, H3.2, and H3.3) have not yet been fully understood. Little is known about the mammalian-specific H3.1 in terms of deposition pattern and role. We show here that the nuclear deposition of these three variants is dynamically changed after fertilization and in the process of embryo preimplantation development, during which genome reprogramming occurs. H3.3, an active gene marker, is removed from the female pronucleus soon after fertilization, suggesting that the epigenetic marks carried by H3.3 in differentiated oocytes are erased. This process might participate in generating totipotency in early embryos. During the late preimplantation stage, H3.1 appears to prevent H3.3 deposition in inactive chromatin domains. The interplay among deposition of H3 variants likely participates in the functional organization of chromatin. Together, our results suggest that dynamic replacement of histone variants plays important roles in genome remodeling.
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影响因子：
64.8
作者：
Hajkova, Petra;Ancelin, Katia;Waldmann, Tanja;Lacoste, Nicolas;Lange, Ulrike C.;Cesari, Francesca;Lee, Caroline;Almouzni, Genevieve;Schneider, Robert;Surani, M. Azim
通讯作者：
Surani, M. Azim
影响因子：
10.5
作者：
Drane, Pascal;Ouararhni, Khalid;Hamiche, Ali
通讯作者：
Hamiche, Ali
DOI：
10.1083/jcb.153.7.1341
发表时间：
2001-06-25
期刊：
The Journal of cell biology
影响因子：
--
作者：
Kimura H;Cook PR
通讯作者：
Cook PR
影响因子：
64.5
作者：
Goldberg AD;Banaszynski LA;Noh KM;Lewis PW;Elsaesser SJ;Stadler S;Dewell S;Law M;Guo X;Li X;Wen D;Chapgier A;DeKelver RC;Miller JC;Lee YL;Boydston EA;Holmes MC;Gregory PD;Greally JM;Rafii S;Yang C;Scambler PJ;Garrick D;Gibbons RJ;Higgs DR;Cristea IM;Urnov FD;Zheng D;Allis CD
通讯作者：
Allis CD
影响因子：
3.7
作者：
Koehler, Daniela;Zakhartchenko, Valeri;Brero, Alessandro
通讯作者：
Brero, Alessandro