DNA methylation reprogramming and DNA repair in the mouse zygote

Lepikhov, Konstantin; Wossidlo, Mark; Arand, Julia; Walter, Joern

doi:10.1387/ijdb.103206kl

Cited by 18 publications

(10 citation statements)

References 119 publications

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“…In mouse zygotes, MatPN maintains H3K9me2 and me3 throughout the first mitotic division just before the two-cell stage. In addition, while MatPN maintains all types of H3 methylation, such as H3K4me1/3, H3K27me2/3, and H4K20me3, patPN remains unmodified until the first DNA replication (Lepikhov et al 2010). These pieces of evidence show that euchromatin may recruit Tet enzymes to patPN as a default state.…”

Section: Discussionmentioning

confidence: 99%

Chromosome-wide regulation of euchromatin-specific 5mC to 5hmC conversion in mouse ES cells and female human somatic cells

et al. 2012

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DNA cytosine methylation (5mC) is indispensable for a number of cellular processes, including retrotransposon silencing, genomic imprinting, and X chromosome inactivation in mammalian development. Recent studies have focused on 5-hydroxymethylcytosine (5hmC), a new epigenetic mark or intermediate in the DNA demethylation pathway. However, 5hmC itself has no role in pluripotency maintenance in mouse embryonic stem cells (ESCs) lacking Dnmt1, 3a, and 3b. Here, we demonstrated that 5hmC accumulated on euchromatic chromosomal bands that were marked with di- and tri-methylated histone H3 at lysine 4 (H3K4me2/3) in mouse ESCs. By contrast, heterochromatin enriched with H3K9me3, including mouse chromosomal G-bands, pericentric repeats, human satellite 2 and 3, and inactive X chromosomes, was not enriched with 5hmC. Therefore, enzymes that hydroxylate the methyl group of 5mC belonging to the Tet family might be excluded from inactive chromatin, which may restrict 5mC to 5hmC conversion in euchromatin to prevent nonselective de novo DNA methylation.Electronic supplementary materialThe online version of this article (doi:10.1007/s10577-012-9317-9) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Chromosome-wide regulation of euchromatin-specific 5mC to 5hmC conversion in mouse ES cells and female human somatic cells

et al. 2012

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“…1). The MII oocyte genome also possesses repressive histone modifications (H3K9me2/3 and H4K20me3) (Lepikhov et al 2010, Hales et al 2011.…”

Section: Genomic Imprinting: a Model For Epigenetic Stabilitymentioning

confidence: 99%

“…The pronuclear paternal genome is rapidly and actively demethylated ( Fig. 1), undergoes protamine to histone replacement, and further acquires active histone modifications (H4Ac, H3Ac, and H3K4me2/3) (Lepikhov et al 2010, Hales et al 2011. By comparison, the maternal pronuclear genome contains active (H4Ac, H3Ac, and H3K4me2/3) and repressive modifications (H3K9me2/3, H3K27me2/ 3, and H4K20me3) and becomes passively demethylated during preimplantation development (Fig.…”

Section: Genomic Imprinting: a Model For Epigenetic Stabilitymentioning

confidence: 99%

Genomic imprints as a model for the analysis of epigenetic stability during assisted reproductive technologies

Denomme¹,

Mann²

2012

Reproduction

112

118

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Gamete and early embryo development are important stages when genome-scale epigenetic transitions are orchestrated. The apparent lack of remodeling of differential imprinted DNA methylation during preimplantation development has lead to the argument that epigenetic disruption by assisted reproductive technologies (ARTs) is restricted to imprinted genes. We contend that aberrant imprinted methylation arising from assisted reproduction or infertility may be an indicator of more global epigenetic instability. Here, we review the current literature on the effects of ARTs, including ovarian stimulation, in vitro oocyte maturation, oocyte cryopreservation, IVF, ICSI, embryo culture, and infertility on genomic imprinting as a model for evaluating epigenetic stability. Undoubtedly, the relationship between impaired fertility, ARTs, and epigenetic stability is unquestionably complex. What is clear is that future studies need to be directed at determining the molecular and cellular mechanisms giving rise to epigenetic errors.

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“…Besides the establishment and the persistence of methylation its removal is also of great biological importance. Demethylation events can occur on a local scale in case of individual gene activation but also on a global genome wide level like in the early zygote and the germ line, where genomes are reprogrammed for new developmental functions [ 11 , 12 ]. In both cases demethylation can be achieved either by an active mechanism (direct removal), a passive replication-dependent loss or a combination of both.…”

Section: Introductionmentioning

confidence: 99%

The Influence of Hydroxylation on Maintaining CpG Methylation Patterns: A Hidden Markov Model Approach

Giehr¹,

Kyriakopoulos

Ficz

et al. 2016

PLoS Comput Biol

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DNA methylation and demethylation are opposing processes that when in balance create stable patterns of epigenetic memory. The control of DNA methylation pattern formation by replication dependent and independent demethylation processes has been suggested to be influenced by Tet mediated oxidation of 5mC. Several alternative mechanisms have been proposed suggesting that 5hmC influences either replication dependent maintenance of DNA methylation or replication independent processes of active demethylation. Using high resolution hairpin oxidative bisulfite sequencing data, we precisely determine the amount of 5mC and 5hmC and model the contribution of 5hmC to processes of demethylation in mouse ESCs. We develop an extended hidden Markov model capable of accurately describing the regional contribution of 5hmC to demethylation dynamics. Our analysis shows that 5hmC has a strong impact on replication dependent demethylation, mainly by impairing methylation maintenance.

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DNA methylation reprogramming and DNA repair in the mouse zygote

Cited by 18 publications

References 119 publications

Chromosome-wide regulation of euchromatin-specific 5mC to 5hmC conversion in mouse ES cells and female human somatic cells

Chromosome-wide regulation of euchromatin-specific 5mC to 5hmC conversion in mouse ES cells and female human somatic cells

Genomic imprints as a model for the analysis of epigenetic stability during assisted reproductive technologies

The Influence of Hydroxylation on Maintaining CpG Methylation Patterns: A Hidden Markov Model Approach

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