DNA methylation profiling of human chromosomes 6, 20 and 22

By F. Eckhardt, Joern Lewin, R. Cortese, Vardhman K. Rakyan, J. Attwood, M. Burger, J. Burton, Tony Cox, R. Davies, Thomas A. Down and 17 more. Nature Genetics, 2006

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DNA methylation is the most stable type of epigenetic modification modulating the transcriptional plasticity of mammalian genomes. Using bisulfite DNA sequencing, we report high-resolution methylation profiles of human chromosomes 6, 20 and 22, providing a resource of about 1.9 million CpG methylation values derived from 12 different tissues. Analysis of six annotation categories showed that evolutionarily conserved regions are the predominant sites for differential DNA methylation and that a core region surrounding the transcriptional start site is an informative surrogate for promoter methylation. We find that 17% of the 873 analyzed genes are differentially methylated in their 5′ UTRs and that about one-third of the differentially methylated 5′ UTRs are inversely correlated with transcription. Despite the fact that our study controlled for factors reported to affect DNA methylation such as sex and age, we did not find any significant attributable effects. Our data suggest DNA methylation to be ontogenetically more stable than previously thought.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/e9c47efee39397d5f1d4d4059c864c44fca004cb

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Citations in the corpus

The epigenomics of cancer. (2007, background): “Indeed, recent DNA methylation profiling of human chromosomes 6, 20, and 22 has shown that 17% of 873 analyzed genes are differentially methylated and that about a third of these show inverse correlations between methylation and transcription (Eckhardt et al., 2006).”
Genome-wide methylation analysis of human colon cancer reveals similar hypo- and hypermethylation at conserved tissue-specific CpG island shores (2009, background): “It has previously been reported that the degree of differences in DNAm of promoters in somatic cells is relatively low in conventionally defined CpG islands and higher at promoters with intermediate CpG densit”
An integrated resource for genome-wide identification and analysis of human tissue-specific differentially methylated regions (tDMRs). (2008, methodology): “Comparison of Batman-called methylation values with bisulfite–PCR sequencing data from the Human Epigenome Project (Eckhardt et al. 2006) and 29 random regions represented on the array used here demonstrates that the”
Preparation of reduced representation bisulfite sequencing libraries for genome-scale DNA methylation profiling (2011, methodology): “Comparisons with other methods In general, methods for DNA methylation mapping fall into three categories: (i) bisulfite-based approaches including RRBS and Illumina (Infinium, GoldenGate) array”
CpG islands – ‘A rough guide’ (2009, methodology): “Recently, DNA ‘‘methylome” characterisation has been the basis for an increasing number of investigations due to significant advances in analytical technologies [1,2,10,29,60].”
A Novel CpG Island Set Identifies Tissue-Specific Methylation at Developmental Gene Loci (2008, background): “Extensive bisulfite sequence analysis [13] surveyed 512 CGIs on Chrs 6, 20, and 21 and reported 9.”
Identification of a CpG island methylator phenotype that defines a distinct subgroup of glioma. (2010, background): “Although this implies that nonrepresentative CpGs may be assessed for some promoters, it is likely that representative results will be obtained for most gene promoters, given the very high degree of locally correlated DNA methylation behavior (Eckhardt et al., 2006).”
CG methylated microarrays identify a novel methylated sequence bound by the CEBPB|ATF4 heterodimer that is active in vivo (2013, background): “Recent global analysis of gene expression and CG methylation has identified many examples of methyla- tion at active promoters (Eckhardt et al. 2006; Weber et al. 2007; Hansen et al. 2011).”
Increased methylation variation in epigenetic domains across cancer types (2011, neutral): “We assumed that p ( L ), the methylation level at location L , was a smooth function of L , meaning proximal CpGs had similar methylation level”
Mapping complex disease traits with global gene expression (2009, background): “For example, non-germ line epigenetic methylation of CpG residues that regulate gene expression is common in the human genom”
The mammalian epigenome. (2007, methodology): “The occurrence of CpG island methylation in these studies is higher than reported in the study by Eckhardt et al. (2006).”
eFORGE: A Tool for Identifying Cell Type-Specific Signal in Epigenomic Data (2016, methodology): “The choice of selecting 1 kb as a limit for filtering was based on previous data showing strong correlation of DNA methylation levels between CpGs fewer than 1 kb apart (Eckhardt et al., 2006).”
Rate, molecular spectrum, and consequences of human mutation (2010, background): “It is common for theCpGswithin human somatic cells to be 20% to 80% methylated (22), although the degree of methylation in germline cells is less clear, and in Drosophila and Caenorhabditis, which do not have detectable levels of methylation, other mechanisms must be responsible for the elevated rat”
Cancer epigenomics: DNA methylomes and histone-modification maps (2007, background): “, and a recent DNA-methylation profile of human chromosomes 6, 20 and 22 (Ref”
Intra-individual change over time in DNA methylation with familial clustering. (2008, background): “In contrast, a recent analysis of about 1 Mb of genomic DNA encompassing 40 000 CpG dinucleotides found no difference in DNA methylation related to age, although those data were based on average values rather than paired sampling in the same individuals over time.(11) To prove that epigenetic marks ”
A Six Months Exercise Intervention Influences the Genome-wide DNA Methylation Pattern in Human Adipose Tissue (2013, neutral): “For example, it was shown that tissue-specific differentially methylated regions in the 59UTR are strongly underrepresented within CpG islands [38] and that most tissue-specific DNA methylation occurs at CpG island shores rather than the within CpG islands, and also in regions more distant than 2 kb”
CpG methylation of half-CRE sequences creates C/EBPα binding sites that activate some tissue-specific genes (2010, background): “Genomic analyses have identified low CpG promoters that are both methylated and transcriptionally active (8, 12), but the mechanism underlying the activation of methylated promoters remains unclear.”