Role of histone methylation in zygotic genome activation in the preimplantation mouse embryo

Shao, Gang; Ding, Hong-Mei; Gong, Aihua

doi:10.1007/s11626-008-9082-4

Cited by 36 publications

(26 citation statements)

References 30 publications

(30 reference statements)

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“…Furthermore, we showed that the rescue of HMGPI had no effect on Klf5 expression in Chd1-knockdown-Hmgpi-rescue embryos, suggesting that there is no direct interaction between Hmgpi and Klf5 during preimplantation development. The maintenance of pluripotency depends on OCT4 and NANOG functions during preimplantation development (Chen et al, 2009;Mitsui et al, 2003;Nichols et al, 1998;Shao et al, 2008). Pou5f1 and Nanog, both of which are ICM markers, negatively interact with Cdx2, a TE marker, and these three genes are key regulators in cell fate specification (Chen et al, 2009;Niwa et al, 2005;Ralston et al, 2010;Strumpf et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

CHD1 acts via the Hmgpi pathway to regulate mouse early embryogenesis

Suzuki

Nozawa

Tsukamoto³

et al. 2015

Development

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The protein CHD1 is a member of the family of ATPase-dependent chromatin remodeling factors. CHD1, which recognizes trimethylated histone H3 lysine 4, has been implicated in transcriptional activation in organisms ranging from yeast to humans. It is required for pre-mRNA maturation, maintenance of mouse embryonic stem cell pluripotency and rapid growth of the mouse epiblast. However, the function(s) of CHD1 in mouse preimplantation embryos has not yet been examined. Here, we show that loss of CHD1 function led to embryonic lethality after implantation. In mouse embryos in which Chd1 was targeted by siRNA microinjection, the expression of the key regulators of cell fate specification Pou5f1 (also known as Oct4), Nanog and Cdx2 was dramatically decreased, starting at mid-preimplantation gene activation (MGA). Moreover, expression of Hmgpi and Klf5, which regulate Pou5f1, Nanog and Cdx2, was also significantly suppressed at zygotic gene activation (ZGA). Suppression of Hmgpi expression in Chd1-knockdown embryos continued until the blastocyst stage, whereas suppression of Klf5 expression was relieved by the morula stage. Next, we rescued HMGPI expression via Hmgpi mRNA microinjection in Chd1-knockdown embryos. Consequently, Pou5f1, Nanog and Cdx2 expression was restored at MGA and live offspring were recovered. These findings indicate that CHD1 plays important roles in mouse early embryogenesis via activation of Hmgpi at ZGA.

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Section: Discussionmentioning

confidence: 99%

CHD1 acts via the Hmgpi pathway to regulate mouse early embryogenesis

Suzuki

Nozawa

Tsukamoto³

et al. 2015

Development

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“…Histone methylation, such as H3K4me2/3, is another key histone modification and is linked with active transcription (Santos-Rosa et al, 2002) and gene activation in zygotes of mice (Shao et al, 2008) and is significant for transcriptional gene reactivation after oocyte reprogramming (Murata et al, 2010). The H3K9me3 histone methylation mark is associated with transcriptional inhibition of euchromatin, repression of chromatin, and formation of heterochromatin.…”

Section: Discussionmentioning

confidence: 99%

Recombinant Human Bone Morphogenetic Protein 6 Enhances Oocyte Reprogramming Potential and Subsequent Development of the Cloned Yak Embryos

Cui

Baloch

et al. 2015

Cellular Reprogramming

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This study investigated the effects of bone morphogenetic protein 6 (BMP6) supplementation in the medium during in vitro maturation (IVM) on the developmental potential of oocytes and in the subsequent development of cloned yak embryos. Cumulus-oocyte complexes (COCs) were aspirated from the antral follicles of yak ovaries and cultured with different concentrations of recombinant human BMP6 in oocyte maturation medium. Following maturation, the metaphase II (MII) oocytes were used for somatic cell nuclear transfer (SCNT), and these were cultured in vitro. The development of blastocysts and cell numbers were detected on day 8. The apoptosis and histone modifications of yak cloned blastocysts were evaluated by detecting the expression of relevant genes and proteins (Bax, Bcl-2, H3K9ac, H3K18ac, and H3K9me3) using relative quantitative RT-PCR or immunofluorescence. The presence of 100 ng/mL BMP6 significantly enhanced the oocyte maturation ratios (66.12 -2.04% vs. 73.11 -1.38%), cleavage rates (69.40 -1.03% vs. 78.16 -0.93%), and blastocyst formation rates (20.63 -1.32% vs. 28.16 -1.67%) of cloned yak embryos. The total blastocysts (85.24 -3.12 vs. 103.36 -5.28), inner cell mass (ICM) cell numbers (19.59 -2.17 vs. 32.20 -2.61), and ratio of ICM to trophectoderm (TE) (22.93 -1.43% vs. 31.21 -1.62%) were also enhanced ( p < 0.05). The ratio of the Bax to the Bcl-2 gene was lowest in the SCNT + BMP6 groups ( p < 0.05). The H3K9ac and H3K18ac levels were increased in SCNT + BMP6 groups ( p < 0.05), whereas the H3K9me3 level was decreased; the differences in blastocysts were not significant ( p > 0.05). These study results demonstrate that addition of oocyte maturation medium with recombinant BMP6 enhances yak oocyte developmental potential and the subsequent developmental competence of SCNT embryos, and provides evidence that BMP6 is an important determinant of mammalian oocyte developmental reprogramming.

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“…It has been determined that the activation occurs at the 2-cell stage in the mouse [14], but transcription actually launches at the late S phase in the 1-cell embryo [15,16]. Our recent studies found that H3K4 hypermethylation results in increased expression of embryonic genes in the 2-and 4-cell stages of mouse embryos [17]. This indicates that histone methylation may be involved in embryonic gene expression.…”

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confidence: 84%

Inheritance of Histone H3 Methylation in Reprogramming of Somatic Nuclei Following Nuclear Transfer

Shao

Ding

Gong

et al. 2008

Journal of Reproduction and Development

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Abstract. Successful cloning requires reprogramming of epigenetic information of the somatic nucleus to an embryonic state. However, the molecular mechanisms regarding epigenetic reprogramming of the somatic chromatin are unclear. Herein, we transferred NIH3T3 cell nuclei into enucleated mouse oocytes and evaluated the histone H3 dimethyl-lysine 4 (H3K4me2) dynamics by immunocytochemistry. A low level of H3K4me2 in the somatic chromatin was maintained in pseudo-pronuclei. Unlike in vitro fertilized (IVF) embryos, the methylation level of nuclear transfer (NT) embryos was significantly increased at the 8-cell stage. NT embryos showed lower H3K4me2 intensity than IVF embryos at the 2-cell stage, which is when the mouse embryonic genome is activated. Moreover, the H3K4me2 signal was weak in the recloned embryos derived from single blastomeres of the NT embryos, whereas it was intense in those from IVF embryos. Two imprinted genes, U2afbp-rs and Xist, were abnormally transcribed in cloned embryos compared with IVF embryos, and this was partly correlated to the H3K4me2 level. Our results suggest that abnormal reprogramming of epigenetic markers such as histone acetylation and methylation may lead to dysregualtion of gene expression in cloned embryos. Key words: Gene expression, Histone H3 methylation, Mouse, Somatic cell nuclear transfer, U2afbp-rs, Xist (J. Reprod. Dev. 54: [233][234][235][236][237][238] 2008) eprogramming of differentiated somatic nuclei to a totipotent state by transfer into oocyte cytoplasm is not efficient. Although in some experiments a considerable proportion of reconstructed embryos might reach the blastocyst stage, the potential developmental ability to full-term is very limited. To improve the efficiency of nuclear transfer (NT), it is necessary to understand the mechanisms of the reprogramming process.The reprogramming events following transfer of somatic nuclei into oocyte cytoplasm occur at the epigenetic level. Histone acetylation and methylation are two important epigenetic modalities [1][2][3][4]. It is known that acetylation of histone plays important roles in transcription activity [5] and histone methylation at K9 associates with gene silencing [6,7]. Recently, histone H3K4 di-methylation (H3K4me2) has been found to be a positive chromatin marker associated with promoters of active genes [8,9]. Similar studies have found that H3K4me3 is enriched at fully activated promoter regions, while H3K4me2 is correlated with the basal transcriptionpermissive state [10]. Demethylation of H3K4 catalyzed by lysinespecific demethylase 1 (LSD1) is associated with transcriptional repression [11]. In addition, H3K4 di-and trimethylation of reprogrammed somatic genomes may be independent of gene activity and may represent one of the major events that occur during somatic genome reprogramming towards a transcriptional activation-permissive state [12].In early embryonic development, activation of the embryonic genome is a crucial event for onset of transcription during preimplantation development [1...

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Role of histone methylation in zygotic genome activation in the preimplantation mouse embryo

Cited by 36 publications

References 30 publications

CHD1 acts via the Hmgpi pathway to regulate mouse early embryogenesis

CHD1 acts via the Hmgpi pathway to regulate mouse early embryogenesis

Recombinant Human Bone Morphogenetic Protein 6 Enhances Oocyte Reprogramming Potential and Subsequent Development of the Cloned Yak Embryos

Inheritance of Histone H3 Methylation in Reprogramming of Somatic Nuclei Following Nuclear Transfer

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