<scp>Cp</scp>
            <scp>G</scp>
            Islands and DNA Methylation

Antequera, Francisco

doi:10.1002/9780470015902.a0005027.pub2

Cited by 7 publications

(6 citation statements)

References 20 publications

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“…This is shown in Figure 1A and B , which compares the frequencies of observed CpG–CpG distances in the human genome ( 33 ) with that expected from a random arrangement of the same number of CpG sites. The distribution of the null model (Figure 1A ) approaches an exponential distribution and there is a small peak at distances close to 10 bp, a distance that is observed in dense regions of CpG sites ( 36 ). However, such analyses only partially capture the clustering of CpGs because they do not address higher order clustering due to correlations between neighboring CpG–CpG distances.…”

Section: Resultsmentioning

confidence: 93%

DNA methylation in human epigenomes depends on local topology of CpG sites

et al. 2016

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In vertebrates, methylation of cytosine at CpG sequences is implicated in stable and heritable patterns of gene expression. The classical model for inheritance, in which individual CpG sites are independent, provides no explanation for the observed non-random patterns of methylation. We first investigate the exact topology of CpG clustering in the human genome associated to CpG islands. Then, by pooling genomic CpG clusters on the basis of short distances between CpGs within and long distances outside clusters, we show a strong dependence of methylation on the number and density of CpG organization. CpG clusters with fewer, or less densely spaced, CpGs are predominantly hyper-methylated, while larger clusters are predominantly hypo-methylated. Intermediate clusters, however, are either hyper- or hypo-methylated but are rarely found in intermediate methylation states. We develop a model for spatially-dependent collaboration between CpGs, where methylated CpGs recruit methylation enzymes that can act on CpGs over an extended local region, while unmethylated CpGs recruit demethylation enzymes that act more strongly on nearby CpGs. This model can reproduce the effects of CpG clustering on methylation and produces stable and heritable alternative methylation states of CpG clusters, thus providing a coherent model for methylation inheritance and methylation patterning.

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Section: Resultsmentioning

confidence: 93%

DNA methylation in human epigenomes depends on local topology of CpG sites

et al. 2016

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“…In vertebrate genomic DNA, the 5' cytosine residues in CpG sequences are often methylated [3]. DNA methylation plays an essential role in the normal development of mammalian embryos by regulating gene expression through genomic imprinting and X chromosome inactivation, and confers genomic stability [4][5][6][7].…”

Section: Epigenetic Regulation By Dna Methylationmentioning

confidence: 99%

Epigenetic Instability in Embryonic Stem Cells

Horii¹,

Hatada²

2013

Pluripotent Stem Cells

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“…DNA methylation in eukaryotes mainly concerns CpG sites (Jaenisch and Bird, 2003 ; Antequera, 2007 ; Portela and Esteller, 2010 ), which are predominantly methylated and sparsely distributed over the genome (Gardiner-Garden and Frommer, 1987 ; Larsen et al, 1992 ; Antequera, 2007 ). However, regions of high CpG density are often unmethylated and located on active promoters (Bird, 1985 ; Larsen et al, 1992 ; Saxonov et al, 2006 ).…”

Section: Introductionmentioning

confidence: 99%

Exploring the Link between Nucleosome Occupancy and DNA Methylation

2018

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Near promoters, both nucleosomes and CpG sites form characteristic spatial patterns. Previously, nucleosome depleted regions were observed upstream of transcription start sites and nucleosome occupancy was reported to correlate both with CpG density and the level of CpG methylation. Several studies imply a causal link where CpG methylation might induce nucleosome formation, whereas others argue the opposite, i.e., that nucleosome occupancy might influence CpG methylation. Correlations are indeed evident between nucleosomes, CpG density and CpG methylation—at least near promoter sites. It is however less established whether there is an immediate causal relation between nucleosome occupancy and the presence of CpG sites—or if nucleosome occupancy could be influenced by other factors. In this work, we test for such causality in human genomes by analyzing the three quantities both near and away from promoter sites. For data from the human genome we compare promoter regions with given CpG densities with genomic regions without promoters but of similar CpG densities. We find the observed correlation between nucleosome occupancy and CpG density, respectively CpG methylation, to be specific to promoter regions. In other regions along the genome nucleosome occupancy is statistically independent of the positioning of CpGs or their methylation levels. Anti-correlation between CpG density and methylation level is however similarly strong in both regions. On promoters, nucleosome occupancy is more strongly affected by the level of gene expression than CpG density or CpG methylation—calling into question any direct causal relation between nucleosome occupancy and CpG organization. Rather, our results suggest that for organisms with cytosine methylation nucleosome occupancy might be primarily linked to gene expression, with no strong impact on methylation.

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Cp G Islands and DNA Methylation

Cited by 7 publications

References 20 publications

DNA methylation in human epigenomes depends on local topology of CpG sites

DNA methylation in human epigenomes depends on local topology of CpG sites

Epigenetic Instability in Embryonic Stem Cells

Exploring the Link between Nucleosome Occupancy and DNA Methylation

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