Epigenetic marks by DNA methylation specific to stem, germ and somatic cells in mice

Shiota, Kunio; Kogo, Yasushi; Ohgane, Jun; Imamura, Takuya; Urano, Atsushi; Nishino, Koichiro; Tanaka, Satoshi; Hattori, Naka

doi:10.1046/j.1365-2443.2002.00574.x

Cited by 188 publications

(191 citation statements)

References 43 publications

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“…There are reports supporting that methylation in these CpG islands regulates gene expression, and that tissue-specific methylation in those provides tissue-specific expression patterns. [14][15][16] However, often the regulation is more complex because there are CpG sites in regulatory regions outside the promoters, and the involvement of modification of the chromatin structure. In fact, the degree of methylation of cytosines 1-2 kb downstream or upstream the islands, so called 'shores', have been found to associate strongly to cell type and to disease, with the shores containing B80% of the regions with tissuespecific methylation.…”

Section: Methylation Of Dnamentioning

confidence: 99%

Epigenetic regulation in obesity

2011

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The availability to the DNA strand and the activity of the transcription machinery is crucial for the cell to use the information in the DNA. The epigenetic mechanisms DNA methylation, modification of histone tails, other chromatin-modifying processes and interference by small RNAs regulate the cell-type-specific DNA expression. Epigenetic marks can be more or less plastic perpetuating responses to various molecular signals and environmental stimuli, but in addition apparently stochastic epigenetic marks have been found. There is substantial evidence from animal and man demonstrating that both transient and more long-term epigenetic mechanisms have a role in the regulation of the molecular events governing adipogenesis and glucose homeostasis. Intrauterine exposure such as poor maternal nutrition has consistently been demonstrated to contribute to a particular epigenotype and thereby developmental metabolic priming of the exposed offspring in animal and man. Epigenetic modifications can be passed not only from one cell generation to the next, but metabolic disease-related epigenotypes have been proposed to also be transmitted germ-line. Future more comprehensive knowledge on epigenetic regulation will complement genome sequence data for the understanding of the complex etiology of obesity and related disorder.

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Section: Methylation Of Dnamentioning

confidence: 99%

Epigenetic regulation in obesity

2011

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“…Bisulfite sequencing was used to determine the methylation the human and mouse may suggest that different mechanisms are involved in the regulation of pluripotency, which require further investigation. Given that the regulation of these genes is tightly correlated to the activity of their promoters, presumably determined by their DNA methylation status, 22,23 we consider it important to investigate the methylation state of such genes in the pig.…”

Section: Oct4mentioning

confidence: 99%

Epigenetic regulation of gene expression in porcine epiblast, hypoblast, trophectoderm and epiblast-derived neural progenitor cells

Gao

Jammes

Rasmussen³

et al. 2011

Epigenetics

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After fertilization, lineage specification is governed by a complicated molecular network in which permissiveness and repression of expression of pluripotency- and differentiation-associated genes are regulated by epigenetic modifications. DNA methylation operates as a very stable repressive mark in this process. In this study, we investigated the relationship between DNA methylation and expression of pluripotency-associated genes (OCT4, NANOG and SOX2), a trophectoderm (TE)-specific gene (ELF5), and genes associated with neural differentiation (SOX2 and VIMENTIN) in porcine Day 10 (E10) epiblast, hypoblast, and TE as well as in epiblast-derived neural progenitor cells (NPCs). We found that OCT4, NANOG, and SOX2 were highly expressed in the epiblast and hypoblast, while VIMENTIN was only highly expressed in the epiblast. Moreover, low expression of OCT4, NANOG, SOX2 and VIMENTIN was noted in the TE. Most CpG sites of OCT4, NANOG, SOX2 and VIMENTIN displayed low methylation levels in the epiblast and hypoblast and, strikingly, also in the TE. Hence, the expression patterns of these genes were not directly related to levels of DNA methylation in the TE in contrast to the situation in the mouse. In contrast, ELF5 was exclusively expressed in the TE and was correspondingly hypomethylated in this tissue. In NPCs, we observed down-regulation of NANOG and OCT4 expression, which correlated with hypermethylation of their promoters, whereas VIMENTIN displayed up-regulation in accordance with hypomethylation of its promoter. In conclusion, DNA methylation is an inconsistently operating epigenetic mechanism in porcine E10 blastocysts, whereas in porcine epiblast-derived NPCs, expression of pluripotency-associated and differentiation genes appear to be regulated by this modification

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“…Methylation and demethylation of the DNA occur during development, establishing distinctive DNA methylation patterns in different cell types (21). Although DNA methylation has been regarded as a relatively stable chromatin mark, a recent report shows that upon activation of ER␣ target genes, CpG dinucleotides of the target promoters undergo cyclical demethylation and remethylation with a frequency of ϳ2 h (22,23), suggesting that this epigenetic mechanism could be involved in dynamic changes in gene expression.…”

Section: Surfactant Protein B (Sftpb)mentioning

confidence: 99%