Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA328818 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3880310.fastq.gz | Fastqsanger.gz | |||
| SRR3880303.fastq.gz | Fastqsanger.gz | |||
| SRR3880304.fastq.gz | Fastqsanger.gz | |||
| SRR3880305.fastq.gz | Fastqsanger.gz | |||
| SRR3880306.fastq.gz | Fastqsanger.gz |
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Project description:MBD4 loss results in global reactivation of promoters and retroelements with low methylated CpG density.
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Project description:Inherited defects in the base-excision repair gene MBD4 predispose individuals to adenomatous polyposis and colorectal cancer, which is characterized by an accumulation of C>T transitions resulting from spontaneous deamination of 5’-methylcytosine. Despite its significance, this DNA repair pathway is still poorly understood. Here we show that the protein MBD4 is required for DNA methylation maintenance and G/T mismatch repair. Transcriptome and methylome analyses reveal a genome-wide hypomethylation of promoters, gene bodies and repetitive elements in the absence of MBD4 in vivo. Methylation mark loss is accompanied by a broad transcriptional derepression phenotype affecting promoters and retroelements with low methylated CpG density. MBD4 in vivo forms a complex with the mismatch repair proteins (MMR), which exhibits high bi-functional glycosylase/AP-lyase endonuclease specific activity towards methylated DNA substrates containing a G/T mismatch. Experiments using recombinant proteins reveal that the association of MBD4 with the MMR protein MLH1 is required for this activity. The described data identify MBD4 as an enzyme specifically designed to repair deaminated 5-methylcytosines and illustrates how MBD4 functions in normal and pathological conditions.
2022-01-10 | GSE84497 | GEO
Project description:Inherited defects in the base-excision repair gene MBD4 predispose individuals to adenomatous polyposis and colorectal cancer, which is characterized by an accumulation of C>T transitions resulting from spontaneous deamination of 5’-methylcytosine. Despite its significance, this DNA repair pathway is still poorly understood. Here we show that the protein MBD4 is required for DNA methylation maintenance and G/T mismatch repair. Transcriptome and methylome analyses reveal a genome-wide hypomethylation of promoters, gene bodies and repetitive elements in the absence of MBD4 in vivo. Methylation mark loss is accompanied by a broad transcriptional derepression phenotype affecting promoters and retroelements with low methylated CpG density. MBD4 in vivo forms a complex with the mismatch repair proteins (MMR), which exhibits high bi-functional glycosylase/AP-lyase endonuclease specific activity towards methylated DNA substrates containing a G/T mismatch. Experiments using recombinant proteins reveal that the association of MBD4 with the MMR protein MLH1 is required for this activity. The described data identify MBD4 as an enzyme specifically designed to repair deaminated 5-methylcytosines and illustrates how MBD4 functions in normal and pathological conditions.
2022-01-10 | GSE84319 | GEO
Project description:Inherited defects in the base-excision repair gene MBD4 predispose individuals to adenomatous polyposis and colorectal cancer, which is characterized by an accumulation of C>T transitions resulting from spontaneous deamination of 5’-methylcytosine. Despite its significance, this DNA repair pathway is still poorly understood. Here we show that the protein MBD4 is required for DNA methylation maintenance and G/T mismatch repair. Transcriptome and methylome analyses reveal a genome-wide hypomethylation of promoters, gene bodies and repetitive elements in the absence of MBD4 in vivo. Methylation mark loss is accompanied by a broad transcriptional derepression phenotype affecting promoters and retroelements with low methylated CpG density. MBD4 in vivo forms a complex with the mismatch repair proteins (MMR), which exhibits high bi-functional glycosylase/AP-lyase endonuclease specific activity towards methylated DNA substrates containing a G/T mismatch. Experiments using recombinant proteins reveal that the association of MBD4 with the MMR protein MLH1 is required for this activity. The described data identify MBD4 as an enzyme specifically designed to repair deaminated 5-methylcytosines and illustrates how MBD4 functions in normal and pathological conditions.
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Project description:We generated RRBS data between Rex1-high and Rex1-low cells to identify differentially methylated promoters. We observe bimodal methylation levels in both subpopulations, and that Rex1-low cells accumulate increased levels of methylation, frequently as a function of local CpG density
2014-07-21 | GSE58396 | GEO
Project description:We generated RRBS data between Rex1-high and Rex1-low cells to identify differentially methylated promoters. We observe bimodal methylation levels in both subpopulations, and that Rex1-low cells accumulate increased levels of methylation, frequently as a function of local CpG density We sorted Rex1 high and low cells using a GFP-knockin reporter cell line (kindly provided by Austin Smith), and performed RRBS on the subpopulations
2014-07-21 | E-GEOD-58396 | biostudies-arrayexpress
Project description:Despite advances in genetics over the last two decades, relating genetic variants to behavior remains a fundamental challenge. Particularly in mice, progress is frustrated by the low resolution of genetic mapping, and consequently by the thousands of candidate causal variants that must be screened. To assess the utility of DNA methylation marks in discovering causative variants we examined their relationship to genetic variation by generating genome-wide, base-pair resolution maps of multiple cell types from the hippocampus of eight fully sequenced inbred strains of Mus musculus. We find that the impact of sequence variation, as mediated by methylation changes, depends on local CpG sequence density. At CpG sequence densities of less than 40 CpG/Kb, cells compensate for loss of methylated sites by methylating additional sites to maintain methylation levels. At higher CpG sequence densities, the exact location of a methylated site becomes more important suggesting that variants affecting methylation sites in regions of high CpG density will have a greater effect on transcription. We test this hypothesis by assessing the effect of mutations on single cell transcript abundance for two inbred strains (C57BL/6J and DBA/2J). The effect of mutations that alter methylated CpG sites is restricted to regions of high sequence density, and from single cell ATAC-seq data, localizes predominantly to enhancers. With approximately tenfold fewer mutations in high than low sequence density CpG regions, candidate variants affecting transcript abundance, and hence downstream phenotypes, including behavior, can be prioritized based on CpG sequence density. Furthermore, our findings imply that DNA methylation influences the likelihood that mutations occur at specific sites in the genome, supporting the view that the distribution of mutations is not random.
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Project description:Epigenetic modification plays important roles in plant and animal development. DNA methylation can impact the transposable element (TE) silencing, gene imprinting and regulate gene expression.Through a genome-wide analysis, DNA methylation peaks were respectively characterized and mapped in maize embryo and endosperm genome. Distinct methylation level across maize embryo and endosperm was observed. The maize embryo genome contained more DNA methylation peaks than endosperm. However, the endosperm chloroplast genome contained more DNA methylation peaks to compare with the embryo chloroplast genome. DNA methylation regions were characterized and mapped in genome. More CG island (CGI) shore are methylated than CGI in maize suggested that DNA methylation level is not positively correlated with CpG density. The DNA methylation occurred more frequently in the promoter sequence and transcriptional termination region (TTR) than other regions of the genes. The result showed that 99% TEs we characterized are methylated in maize embryo, but some (34.8%) of them are not methylated in endosperm. Maize embryo and endosperm exhibit distinct pattern/level of methylation. The most differentially methylated two regions between embryo and endosperm are High CpG content promoters (HCPs) and high CpG content TTRs (HCTTRs). DNA methylation peaks distinction of mitochondria and chloroplast DNA were less than the nucleus DNA. Our results indicated that DNA methylation is associated with the gene silencing or gene activation in maize endosperm and embryo. Many genes involved in embryogenesis and seed development were found differentially methylated in embryo and endosperm. We found 17 endosperm-specific expressed imprinting genes were hypomethylated in endosperm and were hypermethylated in embryo. The expression of a maize DEMETER -like (DME-like) gene and MBD101 gene (MBD4 homolog) which direct bulk genome DNA demethylation were higher in endosperm than in embryo. These two genes may be associated with the distinct methylation level across maize embryo and endosperm.The methylomes of maize embryo and endosperm was obtained by MeDIP-seq method. The global mapping of maize embryo and endosperm methylation in this study broadened our knowledge of DNA methylation patterns in maize genome, and provided useful information for future studies on maize seed development and regulation of metabolic pathways in different seed tissues. Examination of DNA methylated modifications in 2 maize tissues.
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