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Effects of XPC overexpression on global methylation

ABSTRACT: The study examines the impact of XPC overexpression on DNA demethylation in human dermal fibroblasts (HDFs) and during the early phase of somatic cell reprogramming (pre-iPSCs). We profiled the 5mC status in wild type and XPC gain-of-function HDFs and pre-iPSCs on a genome-wide scale by MeDIP-seq. XPC overexpression results in a loss of DNA methylation in both HDFs and pre-iPSCs. In XPC gain-of-function cells, not only does DNA methylation occur in fewer regions compared to control WT cells, but overall methylation levels are lower than in WT cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE92445 | GEO | 2017/05/22

SECONDARY ACCESSION(S): PRJNA357592

REPOSITORIES: GEO

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Homo sapiens

Project description:Effects of XPC overexpression on global methylation

| PRJNA357592 | ENA

Expression data in human oral mucosa fibroblasts (hOFs), dermal fibroblasts, and hOFs-derived iPS cells

Project description:To define the characteristics of human oral mucosa fibroblasts (hOFs), we analyzed the gene expression of hOFs compared with that of human dermal fibroblasts (hDFs), and that of hOF-derived induced pluripotent stem cells (hOF-iPSCs). In this dataset, we found that 5,738 probes and 5672 probes were differently expressed in hOFs and hDFs respectively, compared with those in hOF-iPSCs at more than 2-fold levels. In contrast, only 434 probes are differently expressed between hOFs and hDFs.

2016-04-21 | GSE56805 | GEO

Regulation of DNA methylation landscape in human somatic cell reprogramming by miR-29 family (MeDIP-seq)

Project description:Reprogramming to pluripotency after overexpression of OCT4, SOX2, KLF4 and MYC is accompanied by global genomic and epigenomic changes. Histone modification and DNA methylation states in iPSCs have been shown to be highly similar with embryonic stem cells (ESCs). However, epigenetic differences still exist between iPSCs and ESCs. In particular, aberrant DNA methylation states found in iPSCs are a major concern for using iPSCs in a clinical setting. Thus, it is critical to find factors that regulate DNA methylation states in reprogramming. Here, we found that the miR-29 family is an important epigenetic regulator during human somatic cell reprogramming. Our global DNA methylation and hydroxymethylation analysis shows that DNA demethylation is a major event mediated by miR-29a depletion during early reprogramming, and that iPSCs derived from miR-29a depletion are epigenetically closer to ESCs. Our findings uncover an important miRNA-based approach to generate clinically robust iPSCs.

2016-05-24 | GSE81793 | GEO

Regulation of DNA methylation landscape in human somatic cell reprogramming by miR-29 family (RNA-seq)

2016-05-24 | GSE81791 | GEO

Regulation of DNA methylation landscape in human somatic cell reprogramming by miR-29 family (illumina 450K)

2016-05-24 | GSE81790 | GEO

Transcriptional analysis of pre and post excision human induced pluripotent stem cells

Project description:Transcriptional analysis was performed on pre and post excision human induced pluripotent stem cells, the donor human dermal fibroblasts (HDFs) they were derived from and control human embryonic stem cells We isolated total RNA from pre and post excision human induced pluripotent stem cells, the donor human dermal fibroblasts (HDFs) they were derived from and control human embryonic stem cells and analyzed via Affymetrix microarray analysis.

2013-07-13 | E-GEOD-48830 | biostudies-arrayexpress

An XPC-PARP axis links ALC1-mediated chromatin remodeling to global genome DNA damage repair

Project description:Cells employ global genome DNA damage repair (GGR) to eliminate a broad spectrum of DNA lesions, including those induced by UV light. The lesion-recognition factor XPC initiates repair of helix-distorting DNA lesions, but binds inefficiently to lesions that cause poor helix distortion. How such difficult-to-repair lesions are detected in chromatin is unknown. Here, we identify the poly-(ADP-ribose) polymerases PARP1 and PARP2 as constitutive interactors of XPC. The close interaction between these proteins results in the PARylation of XPC at UV lesions, and an XPC-dependent stimulation of the poly-(ADP-ribose) response, which facilitates the recruitment of the poly-(ADP-ribose)-dependent chromatin remodeler ALC1. Both ALC1 and in particular PARP2 are required for the efficient clearing of difficult-to-repair DNA lesions. Our study offers key insights into the molecular mechanisms of GGR by revealing a molecular bookmarking system, which primes chromatin containing difficult-to-repair DNA lesions for efficient repair.

2022-07-15 | PXD025226 | Pride

X Chromosome Dosage Influences DNA Methylation Dynamics During Reprogramming to Mouse iPSCs

Project description:A dramatic difference in global DNA methylation between male and female cells characterizes mouse embryonic stem cells (ESCs), unlike somatic cells. We analyzed DNA methylation changes during reprogramming of male and female somatic cells and in resulting induced pluripotent stem cells (iPSCs). At an intermediate reprogramming stage, somatic and pluripotency enhancers are targeted for partial methylation and demethylation. Demethylation within pluripotency enhancers often occurs at ESC binding sites of pluripotency transcription factors. Late in reprogramming, global hypomethylation is induced in a female-specific manner. Genome-wide hypomethylation in female cells affects many genomic landmarks, including enhancers and imprint control regions, and accompanies the reactivation of the inactive X-chromosome. The loss of one of the two X-chromosomes in propagating female iPSCs is associated with genome-wide methylation gain. Collectively, our findings highlight the dynamic regulation of DNA methylation at enhancers during reprogramming and reveal that X-chromosome dosage dictates global DNA methylation levels in iPSCs.

2018-04-19 | GSE111042 | GEO

The C-terminal region of Xpc is dispensable for the transcriptional activity of Oct3/4 in mouse embryonic stem cells

Project description:The transcription factor Oct3/4 is essential to maintain pluripotency in mouse embryonic stem (ES) cells. It was reported that the Xpc DNA repair complex is involved in this process. Here we examined the role of Xpc on the transcriptional activation of the target genes by Oct3/4 using the inducible knockout strategy. We found that the removal of the C-terminal region of Xpc, including the interaction sites with Rad23 and Cetn2, showed faint impact on the gene expression profile of ES cells and the functional Xpc-ΔC ES cell lines retained proper gene expression profile as well as pluripotency to contribute chimeric embryos. These data indicated that the C-terminal region of Xpc is dispensable for the transcriptional activity of Oct3/4 in mouse ES cells. An inducible knockout ES cell line of Xpc with the Cre-loxP system was generated and gene expression was measured without Xpc deletion, after 4 days of Xpc deletion or constitutive knocked out cells. Each sample was prepared in triplicate.

2015-06-09 | E-GEOD-69640 | biostudies-arrayexpress

Functional and Mechanistic Studies of XPC DNA-Repair Complex as Transcriptional Coactivator in Embryonic Stem Cells

Project description:We recently identified the DNA repair complex XPC-RAD23B-CETN2 as a stem cell coactivator (SCC) required for OCT4 and SOX2 transcriptional activation. Here we investigate genome-wide the role of SCC in murine ESCs by mapping regions bound by its RAD23B subunit in wild type and Xpc-/- ESCs, and analyzing transcriptional profiles of SCC-depleted ESCs. RAD23B ChIP-seq in wild type murine ESCs was performed in two replicates; normal IgG were used as controls. RAD23B ChIP-seq in Xpc-/- mESCs was compared to normal IgG. Antibodies to immunoprecipitate RAD23B were raised in guinea pigs against the 108-177 peptide of murine RAD23B protein (NP_033037). Anti-sera were affinity-purified. For RNA-seq, we compared wild type JM8.N4 cells with either Rad23b-/- cells, Rad23b-/-Xpc KD1 or Rad23b-/-Xpc KD2 cells. Xpc was knocked down with two independent shRNAs (KD1 and KD2).

2015-04-20 | E-GEOD-64040 | biostudies-arrayexpress

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