Genome-wide methylated CpG status in WT and IRF8KO microglia [WGBS]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA964777 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24386470_1.fastq.gz | Fastqsanger.gz | |||
| SRR24386470_2.fastq.gz | Fastqsanger.gz | |||
| SRR24386471_1.fastq.gz | Fastqsanger.gz | |||
| SRR24386471_2.fastq.gz | Fastqsanger.gz | |||
| SRR24386472_1.fastq.gz | Fastqsanger.gz |
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Project description:The role of the lineage-determining transcription factor, Interferon regulatory factor (IRF8), in microglia remains elucidated. We report the genome-wide methyl-CpG status in adult wild-type (WT) and IRF8-knockout (IRF8KO) microglia by whole-genome bisulfite-Seq (WGBS). Deep-sequencing and subsequent differential analysis revealed that IRF8KO microglia exhibited a cell-intrinsic methylation profile. Furthermore, the differentially methylated regions showed a significant correlation with IRF8-dependent chromatin accessibility in microglia. This study provides a novel insight into understanding epigenetic regulation in microglia.
2023-06-01 | GSE231404 | GEO
Project description:The role of the lineage-determining transcription factor, Interferon regulatory factor (IRF8), in microglia remains unelucidated. We report the genome-wide chromatin status in adult wild-type (WT) and IRF8-knockout (IRF8KO) microglia by ATAC-Seq. Deep-sequencing and subsequent differential analysis revealed that chromatin accessibility in microglia requires IRF8. At the same time, the loss of IRF8 gains aberrant chromatin accessibility that potentially confers mRNA transcription of the genes upregulated in IRF8KO microglia. This study provides a novel insight into understanding epigenetic regulation in microglia.
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Project description:The role of a transcription factor, Interferon Regulatory Factor 8 (IRF8), in microglia is yet to be fully understood. We conducted a study to examine the chromatin status of postnatal and adult wild-type (WT) and IRF8-knockout (IRF8KO) microglia through ATAC-Seq. We also added 5xFAD Alzheimer's disease microglia to observe any chromatin events that may be similar in disease-associated microglia. After deep-sequencing and differential analysis, we discovered that chromatin accessibility in microglia is dependent on IRF8. In the absence of IRF8, there was aberrant chromatin accessibility that potentially resulted in mRNA transcription of genes that were upregulated in IRF8KO microglia, which was distinct from 5xFAD microglia. This study contributes to a better understanding of epigenetic regulation in microglia.
2024-07-01 | GSE266421 | GEO
Project description:Genome-wide open chromatin status in WT and IRF8KO microglia
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Project description:Genome-wide open chromatin status in WT and IRF8KO microglia [ATAC-seq]
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Project description:The role of the lineage-determining transcription factor IRF8 in microglia remains unelucidated. We report the genome-wide, transcriptome profiles of wild-type, IRF8KO, IRF8cKO, Batf3KO, 5xFAD, and 5xFAD/IRF8KO microglia. Deep-sequencing and subsequent differential analysis revealed the impacts of IRF8 on microglia-specific transcription programs, such as cell identity. Sall1 and Batf3 genes were identified as a downstream transcription factor of IRF8, and Batf3 dependent genes showed correlation with IRF8-dependent genes in microglia. The conditional depletion of IRF8 gene after microglial maturation (P14) increased or decreased the gene expression, most of which were shared with those of IRF8KO. This study provides a novel insight into understanding transcriptional programs in microglia.
2023-06-01 | GSE231403 | GEO
Project description:We wanted to emphisize the role of intragenic CpG island in various cell differentiation. We especially examined the effect of DNA methyltransferase (DNMT) in the neural differentiation from mouse ES cell. Therefore, we performed the Whole-Genome Bisulfite Sequencing (WGBS) analysis of mouse ES cell, ESC-derived NPC, and also in DNMT double knockout (DKO) conditions. By utilizing these result, we confirmed the genes regulated by intragenic CpG island methylation have effect in NPC differentation.
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Project description:To globally define methylation-M-bM-^@M-^YproneM-bM-^@M-^Y and -M-bM-^@M-^YprotectedM-bM-^@M-^Y CpG islands in cancer, we analyzed the methylation status of 23,000 CpG islands of the human genome in 19 colorectal carcinoma samples as well as normal colon using our previously described methyl-CpG immunoprecipitation (MCIp) technique (Gebhard et al. 2006; Schilling and Rehli 2007). This method enriches for highly CpG methylated DNA that can be directly applied to fluorescent labeling and oligonucleotide microarray hybridization without an additional amplification step. CpG-methylated genomic DNA was enriched using methyl-CpG immunoprecipitation (MCIp). On each microarray, the enriched material from colorectal carcinoma samples was compared to the enriched material from normal colon to identify aberrantly methylated regions.
2012-11-01 | E-GEOD-25221 | biostudies-arrayexpress
Project description:To globally define methylation-’prone’ and -’protected’ CpG islands in cancer, we analyzed the methylation status of 23,000 CpG islands of the human genome in 19 colorectal carcinoma samples as well as normal colon using our previously described methyl-CpG immunoprecipitation (MCIp) technique (Gebhard et al. 2006; Schilling and Rehli 2007). This method enriches for highly CpG methylated DNA that can be directly applied to fluorescent labeling and oligonucleotide microarray hybridization without an additional amplification step.
2012-11-01 | GSE25221 | GEO
Project description:Determination of the profile of genes commonly aberrantly methylated in colorectal cancer (CRC) has substantial potential value for diagnostic and therapeutic application. However, our knowledge of the DNA methylation pattern in CRC is currently limited. Therefore, we analyzed the methylation profile of 27,578 CpG sites spanning more than 14,000 genes in CRC and in adjacent normal mucosa using beadchip array-based technology. We identified 621 CpG sites located in promoter region and CpG islands that were significantly hypermethylated in CRC compared to normal mucosa. Genes on chromosome 18 showed promoter hypermethylation most frequently. According to gene ontology analysis, the most common biologically relevant class of genes affected by methylation was the class associated with the cadherin signaling pathway. In comparison with genome-wide expression array, mRNA expression was more like to be down-regulated in the genes demonstrating promoter hypermethylation, although this was not statistically significant. We validated 10 CpG sites that were shown to be hypermethylated in the array studies (ADHFE1, BOLL, SLC6A15, ADAMTS5, TFPI2, EYA4, NPY, TWIST1, LAMA1, GAS7) and 2 CpG sites showing hypomethylaion (MAEL, SFT2D3) in CRC compared to normal mucosa using pyrosequencing. The methylation status measured by pyrosequencing was consistent with the methylation array data. In conclusion, we have shown that methylation profiling based on beadchip arrays is an effective method for screening for aberrantly methylated genes in CRC. In addition, we identified novel methylated genes that are candidate diagnostic or prognostic markers for CRC. We measured the methylation status of the 27,578 CpG sites (Human Methylation27 DNA Analysis BeadChip) in 22 pairs of CRC tissue and adjacent normal mucosa to identify genes that are commonly aberrantly methylated in CRC.
2010-06-24 | E-GEOD-17648 | biostudies-arrayexpress