<i>De Novo</i> DNA methylation independent establishment of maternal imprint on X chromosome in mouse oocytes

Chiba, Hayato; Hirasawa, Ryutaro; Kaneda, Masahiro; Amakawa, Yuko; Li, En; Sado, Takashi; Sasaki, Hidetada

doi:10.1002/dvg.20496

Cited by 6 publications

(5 citation statements)

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“…Our conditional knockout mice should be useful for investigating the molecular mechanisms that establish the maternal imprints in oocytes. Indeed, we have recently used these mice to explore the mechanisms of imprinting of maternal X‐chromosome and contribution of the oocyte‐derived Dnmts in the maintenance of autosomal imprints in preimplantation embryos (Chiba et al. 2008; Hirasawa et al.…”

Section: Discussionmentioning

confidence: 99%

Genetic evidence for Dnmt3a‐dependent imprinting during oocyte growth obtained by conditional knockout with Zp3‐Cre and complete exclusion of Dnmt3b by chimera formation

et al. 2010

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In the male and female germ-lines of mice, both of the two de novo DNA methyltransferases Dnmt3a and Dnmt3b are expressed. By the conditional knockout experiments using the TnapCre gene, we previously showed that deletion of Dnmt3a in primordial germ cells disrupts paternal and maternal imprinting, however, Dnmt3b mutants did not show any defect. Here, we have knocked out Dnmt3a after birth in growing oocytes by using the Zp3-Cre gene and obtained genetic evidence that de novo methylation by Dnmt3a during the oocyte growth stage is indispensable for maternal imprinting. We also carried out DNA methylation analysis in the mutant oocytes and embryos and found that hypomethylation of imprinted genes in Dnmt3a-deficient oocytes was directly inherited to the embryos, but repetitive elements were re-methylated during development. Furthermore, we show that Dnmt3b-deficient cells can contribute to the male and female germ-lines in chimeric mice and can produce normal progeny, establishing that Dnmt3b is dispensable for mouse gametogenesis and imprinting. Finally, Dnmt3-related protein Dnmt3L is not only essential for methylation of imprinted genes but also enhances de novo methylation of repetitive elements in growing oocytes.

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Section: Discussionmentioning

confidence: 99%

Genetic evidence for Dnmt3a‐dependent imprinting during oocyte growth obtained by conditional knockout with Zp3‐Cre and complete exclusion of Dnmt3b by chimera formation

et al. 2010

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“…Indeed, in Robertsonian translocations in which zygotes with two maternal X chromosomes were generated, both remained active in the early embryo and the trophoblast (Goto and Takagi, 1998). The nature of this maternal imprint is unknown, but it was shown not to require acquisition of de novo DNA methylation (Chiba et al, 2008). In mice, the epigenetic maternal imprint could possibly activate expression of Tsix, an antisense transcript that prevents expression of Xist RNA.…”

Section: Developmental Cellmentioning

confidence: 99%

Epigenetic Transitions in Germ Cell Development and Meiosis

2010

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Germ cell development is controlled by unique gene expression programs and involves epigenetic reprogramming of histone modifications and DNA methylation. The central event is meiosis, during which homologous chromosomes pair and recombine, processes that involve histone alterations. At unpaired regions, chromatin is repressed by meiotic silencing. After meiosis, male germ cells undergo chromatin remodeling, including histone-to-protamine replacement. Male and female germ cells are also differentially marked by parental imprints, which contribute to sex determination in insects and mediate genomic imprinting in mammals. Here, we review epigenetic transitions during gametogenesis and discuss novel insights from animal and human studies.

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“…Previous studies using nuclear transfer approaches have suggested that genomic imprinting of Xist is established during oogenesis (Tada et al 2000;Oikawa et al 2014). However, analyses of DNA methyltransferase maternal knockout embryos revealed that oocyte DNA methylation is dispensable for Xist imprinting (Chiba et al 2008). A recent study demonstrated that overexpression of an H3K9me3 demethylase, Kdm4b, in parthenogenetic (PG) embryos partially derepresses Xist (Fukuda et al 2014), suggesting the involvement of H3K9me3 in imprinted Xist silencing.…”

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Genomic imprinting of Xist by maternal H3K27me3

et al. 2017

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Maternal imprinting at the gene is essential to achieve paternal allele-specific imprinted X-chromosome inactivation (XCI) in female mammals. However, the mechanism underlying imprinting is unclear. Here we show that the locus is coated with a broad H3K27me3 domain that is established during oocyte growth and persists through preimplantation development in mice. Loss of maternal H3K27me3 induces maternal expression and maternal XCI in preimplantation embryos. Our study thus identifies maternal H3K27me3 as the imprinting mark of .

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De Novo DNA methylation independent establishment of maternal imprint on X chromosome in mouse oocytes

Cited by 6 publications

References 0 publications

Genetic evidence for Dnmt3a‐dependent imprinting during oocyte growth obtained by conditional knockout with Zp3‐Cre and complete exclusion of Dnmt3b by chimera formation

Genetic evidence for Dnmt3a‐dependent imprinting during oocyte growth obtained by conditional knockout with Zp3‐Cre and complete exclusion of Dnmt3b by chimera formation

Epigenetic Transitions in Germ Cell Development and Meiosis

Genomic imprinting of Xist by maternal H3K27me3

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