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The effect of genotype and in utero environment on inter-individual variation in neonate DNA methylomes (methylomes)

ABSTRACT: We surveyed the genotypes and DNA methylomes of 237 neonates and found 1423 punctate regions of the methylome that were highly variable across individuals, termed variably methylated regions (VMRs), against a backdrop of homogeneity. Although methQTLs were readily detected in neonatal methylomes, genotype alone did not explain the majority of the VMRs. We found that the best explanation for 75% of VMRs was the interaction of genotype with different in utero environments, including maternal smoking, maternal depression, maternal BMI, infant birth weight, gestational age and birth order.

ORGANISM(S): Homo sapiens

PROVIDER: GSE53816 | GEO | 2014/04/02

SECONDARY ACCESSION(S): PRJNA236558

REPOSITORIES: GEO

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The effect of genotype and in utero environment on inter-individual variation in neonate DNA methylomes (genotypes)

Project description:We surveyed the genotypes and DNA methylomes of 237 neonates and found 1423 punctate regions of the methylome that were highly variable across individuals, termed variably methylated regions (VMRs), against a backdrop of homogeneity. Although methQTLs were readily detected in neonatal methylomes, genotype alone did not explain the majority of the VMRs. We found that the best explanation for 75% of VMRs was the interaction of genotype with different in utero environments, including maternal smoking, maternal depression, maternal BMI, infant birth weight, gestational age and birth order.

2014-04-02 | GSE54445 | GEO

The effect of genotype and in utero environment on inter-individual variation in neonate DNA methylomes

2014-04-02 | E-GEOD-53816 | biostudies-arrayexpress

The effect of genotype and in utero environment on inter-individual variation in neonate DNA methylomes

2014-04-02 | E-GEOD-54445 | biostudies-arrayexpress

Programming and inheritance of parental DNA methylomes in mammals

2014-05-12 | GSE56697 | GEO

Programming and inheritance of parental DNA methylomes in mammals

Project description:The reprogramming of parental methylomes is essential for embryonic development. In mammals, paternal 5-methylcytosines (5mCs) have been proposed to be actively converted to oxidized bases. These paternal oxidized bases and maternal 5mCs are believed to be passively diluted by cell divisions. By generating single-base resolution, allele-specific DNA methylomes from mouse gametes, early embryos, and primordial germ cell (PGC), as well as single-base-resolution maps of oxidized cytosine bases for early embryos, we report the existence of 5hmC and 5fC in both maternal and paternal genomes and find that 5mC or its oxidized derivatives, at the majority of demethylated CpGs, are converted to unmodified cytosines independent of passive dilution from gametes to four-cell embryos. Therefore, we conclude that paternal methylome and at least a significant proportion of maternal methylome go through active demethylation during embryonic development. Additionally, all the known imprinting control regions (ICRs) were classified into germ-line or somatic ICRs. The cross of two mouse strains was performed using DBA/2J as the paternal strain and C57BL/6J as the maternal strain. The hybrid embryos were collected at 2-cell, 4-cell, ICM, E6.5, E7.5 stages. Female and male E13.5 PGC samples (B6; 129S4-Pou5f1tm2Jae/J) were collected from timed mating of C57BL/6J female mice. MethylC-Seq: oocytes (C57BL/6J), sperm (DBA/2J), 2-cell embryos, 4-cell embryos, ICM, E6.5 embryos, E7.5 embryos, E13.5 female PGCs and E13.5 male PGCs. TAB-Seq: 2-cell embryos. fCAB-Seq: 2-cell embryos. RNA-Seq: oocytes (C57BL/6J).

2014-05-12 | E-GEOD-56697 | biostudies-arrayexpress

Bisulfite sequencing of medaka PGCs methylomes

Project description:Medaka PGCs methylomes were sequenced using whole genome bisulfite sequencing (WGBS)

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Project description:Medaka sperm methylomes were sequenced using whole genome bisulfite sequencing (WGBS)

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Mapping of variable DNA methylation across multiple cell types defines a dynamic regulatory landscape of the human genome

Project description:DNA methylation is an important epigenetic modification involved in many biological processes and diseases. Many studies have mapped DNA methylation changes associated with embryogenesis, cell differentiation and cancer at a genome-wide scale. Our understanding of genome-wide DNA methylation changes in a developmental or disease-related context has been steadily growing. However, the investigation of which CpGs are variably methylated in different normal cell or tissue types is still limited. Here we present an in-depth analysis of 54 single-CpG-resolution DNA methylomes of normal human cell types by integrating high-throughput sequencing-based methylation data. We find that the percentage of unmethylated CpGs is relatively fixed regardless of cell type. However, which CpGs are unmethylated is cell-type specific. We categorize the 26 million human autosomal CpGs based on their methylation levels across multiple cell types to identify variably methylated CpGs. Among all the autosomal CpGs, 22.6% exhibit variable DNA methylation across cell types included in our study. These variably methylated CpGs form 66 thousand variably methylated regions (VMRs), encompassing 11% of the genome. By integrating a multitude of genomic data, we found that VMRs enrich for histone modifications indicative of enhancers, suggesting their role as regulatory elements marking cell type specificity. VMRs enrich for transcription factor binding sites in a tissue-dependent manner. Importantly, they enrich for GWAS variants, suggesting VMRs could potentially be implicated in disease and complex traits. Taken together, our results highlight the link among CpG methylation variation, genetic variation and disease risk in a tissue-specific manner for many human cell types. Processed data includes new Samples and 75 Samples from GSE16368 and 2 Samples from GSE51565.

2016-04-06 | E-GEOD-69894 | biostudies-arrayexpress

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