Crosstalk between gene body DNA methylation, H3K9me3 and H3K36me3 chromatin marks and transcription
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Xiwei Wu
PROVIDER: E-GEOD-26020 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:This is one of expressional parts of the study. These data were correlated to epigenetic changes and CG density of genes in analyzed cells. The whole study has a following summary: To elucidate possible roles of DNA methylation and chromatin marks in transcription, we performed epigenetic profiling of chromosome 19 in human bronchial epithelial cells (HBEC) and in the colorectal cancer cell line HCT116 as well as its counterpart with double knockout of DNMT1 and DNMT3B (HCT116-DKO). We found that H3K9me3 forms intragenic chromatin blocks along genes with low CpG density in the gene body. Analysis of H3K36me3 profiles indicated that this mark associates either with active genes with low CpG density and H3K9me3 in the gene body or with active genes with high CpG density and DNA hypermethylation in the gene body. In HCT116 cells with double knockout of DNMT1 and DNMT3B, transcription of genes with low CpG density in the gene body was highly elevated and associated with promoter DNA demethylation and rearrangement of H3K9me3 and H3K36me3 occupation. Our finding suggests that similar to DNA methylation, H3K9me3 may play a role in intragenic gene regulation. Further, we observed that a combination of low CpG density in gene bodies together with H3K9me3 and H3K36me3 marking is a specific epigenetic feature of zinc finger (ZNF) genes, which comprise 90% of all genes carrying both histone marks on chromosome 19. For high CpG density genes, transcription and H3K36me3 occupancy were not changed in condition of partial or intensive loss of DNA methylation in gene bodies in the HCT116-DKO cell line. siRNA experiments with SETD2 knockdown in both HBEC and HCT116-DKO cell lines failed to reduce DNA methylation in gene bodies under conditions of H3K36me3 depletion. Our study suggests that the H3K36me3 and DNA methylation marks in gene bodies are established independently from each other and points to similar functional roles of intragenic DNA methylation and intragenic H3K9me3 for CpG-rich and CpG-poor genes, respectively. To elucidate how a loss of DNA methylation affects a gene expression and epigenome we studied colon cancer cell line HCT116 and its derivative, HCT116 DNMT1-/- DNMT3b -/- (HCT116-DKO). According to previous studies HCT116-DKO is characterized by 95% of loss of DNA methylation. In HCT116 and HCT116-DKO cells, we profiled diverse epigenetic marks and gene expression. Further a crosstalk between epigenetic changes and transcriptional changes was analyzed. This is the expressional part of study.
2011-03-31 | E-GEOD-26018 | biostudies-arrayexpress
Project description:This is one of expressional parts of the study. These data were correlated to epigenetic marks and CG density of genes in analyzed cells. The whole study has a following summary: To elucidate possible roles of DNA methylation and chromatin marks in transcription, we performed epigenetic profiling of chromosome 19 in human bronchial epithelial cells (HBEC) and in the colorectal cancer cell line HCT116 as well as its counterpart with double knockout of DNMT1 and DNMT3B (HCT116-DKO). We found that H3K9me3 forms intragenic chromatin blocks along genes with low CpG density in the gene body. Analysis of H3K36me3 profiles indicated that this mark associates either with active genes with low CpG density and H3K9me3 in the gene body or with active genes with high CpG density and DNA hypermethylation in the gene body. In HCT116 cells with double knockout of DNMT1 and DNMT3B, transcription of genes with low CpG density in the gene body was highly elevated and associated with promoter DNA demethylation and rearrangement of H3K9me3 and H3K36me3 occupation. Our finding suggests that similar to DNA methylation, H3K9me3 may play a role in intragenic gene regulation. Further, we observed that a combination of low CpG density in gene bodies together with H3K9me3 and H3K36me3 marking is a specific epigenetic feature of zinc finger (ZNF) genes, which comprise 90% of all genes carrying both histone marks on chromosome 19. For high CpG density genes, transcription and H3K36me3 occupancy were not changed in condition of partial or intensive loss of DNA methylation in gene bodies in the HCT116-DKO cell line. siRNA experiments with SETD2 knockdown in both HBEC and HCT116-DKO cell lines failed to reduce DNA methylation in gene bodies under conditions of H3K36me3 depletion. Our study suggests that the H3K36me3 and DNA methylation marks in gene bodies are established independently from each other and points to similar functional roles of intragenic DNA methylation and intragenic H3K9me3 for CpG-rich and CpG-poor genes, respectively. Expressional changes associated with SETD2 siRNA transfection in HBEC Compare siRNA vs. control
2011-03-31 | E-GEOD-26038 | biostudies-arrayexpress
Project description:This is one of expressional parts of the study. These data were correlated to epigenetic marks and CG density of genes in analyzed cells. The whole study has a following summary: To elucidate possible roles of DNA methylation and chromatin marks in transcription, we performed epigenetic profiling of chromosome 19 in human bronchial epithelial cells (HBEC) and in the colorectal cancer cell line HCT116 as well as its counterpart with double knockout of DNMT1 and DNMT3B (HCT116-DKO). We found that H3K9me3 forms intragenic chromatin blocks along genes with low CpG density in the gene body. Analysis of H3K36me3 profiles indicated that this mark associates either with active genes with low CpG density and H3K9me3 in the gene body or with active genes with high CpG density and DNA hypermethylation in the gene body. In HCT116 cells with double knockout of DNMT1 and DNMT3B, transcription of genes with low CpG density in the gene body was highly elevated and associated with promoter DNA demethylation and rearrangement of H3K9me3 and H3K36me3 occupation. Our finding suggests that similar to DNA methylation, H3K9me3 may play a role in intragenic gene regulation. Further, we observed that a combination of low CpG density in gene bodies together with H3K9me3 and H3K36me3 marking is a specific epigenetic feature of zinc finger (ZNF) genes, which comprise 90% of all genes carrying both histone marks on chromosome 19. For high CpG density genes, transcription and H3K36me3 occupancy were not changed in condition of partial or intensive loss of DNA methylation in gene bodies in the HCT116-DKO cell line. siRNA experiments with SETD2 knockdown in both HBEC and HCT116-DKO cell lines failed to reduce DNA methylation in gene bodies under conditions of H3K36me3 depletion. Our study suggests that the H3K36me3 and DNA methylation marks in gene bodies are established independently from each other and points to similar functional roles of intragenic DNA methylation and intragenic H3K9me3 for CpG-rich and CpG-poor genes, respectively. Expression profile of human bronchial epithelia cells (HBEC) immortalized with hTERT and CDK4. To elucidate possible roles of DNA methylation and chromatin marks in transcription, we performed epigenetic profiling of chromosome 19 in human bronchial epithelial cells (HBEC) and analyzed gene expression by Affymetrix expression arrays in these cells. This is the expressional part of study.
2011-03-31 | E-GEOD-26019 | biostudies-arrayexpress
Project description:Crosstalk between gene body DNA methylation, H3K9me3 and H3K36me3 chromatin marks and transcription [HuEx-1_0-st]
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Project description:Crosstalk between gene body DNA methylation, H3K9me3 and H3K36me3 chromatin marks and transcription [HuEx-1_0-st, transcript]
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Project description:Crosstalk between gene body DNA methylation, H3K9me3 and H3K36me3 chromatin marks and transcription [HuGene-1_0-st]
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Project description:Analysis of cross talk of epigenetic marks in HBEC by using tilling arrays chr19. In Human Bronchial epithelia cells (HBEC), H3K9me3, H4K20me3, H3K4me3, H3K27me3, H3K36me3 and DNA methylation were profiled. In these cells, DNA methylation status was analyzed by MIRA and UnmethylCollector (UMC). Study of epigenetic changes in HCT116 DNMT1-/- and DNMT3b -/- (HCT116-DKO) in comparison to intact HCT116. In HCT116 and HCT116-DKO, H3K9me3, H3K36me3 and DNA methylation were profiled. In these cells, DNA methylation status was analyzed by MIRA. Analysis of epigenetic changes caused by siRNA for SED2 transcript in HBEC. In HBEC and SETD2 siRNA HBEC, H3K36me3 and DNA methylation were profiled. In these cells, DNA methylation status was analyzed by MIRA. Comapre DNA methylation and other histone modification marks
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2007-10-19 | E-GEOD-9342 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE36084: Gene expression data from human lymphocytes GSE36397: ChIP-chip of monocytes using H3K9Ac, H3K4me3, H3K9me2 and H4K16Ac antibodies GSE36402: ChIP-chip of lymphocytes using H3K9Ac, H3K4me3, H3K9me3, H3K27me3 and H4K16Ac antibodies Refer to individual Series
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