ChIP-seq DNA libraries were constructed by HNRNPK antibody to immunoprecipitate the fragment DNA in H1299 cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE197777 | GEO | 2022/03/09
REPOSITORIES: GEO
Similar Datasets
Project description:Purpose: To identify nucleosome-depleted regions in response to drought in the kidney bean, a genome-wide chromatin profiling strategy was implemented. A better understanding of these OCRs (Open chromatin regions) will be useful in exploring potential genomic regions for crop improvement. Results: Using a comprehensive FAIRE-Seq approach, nucleosome-free chromatin regions were explored in kidney bean (Phaseolus vulgaris. L) in response to both drought and rewatering stress. In all samples, FAIRE peaks (>50%) were enriched in the promoter regions. The drought samples showed peaks very distinct from control and rewatered samples, which showed peaks predominantly at the transcription start site (TSS). Drought and heat-responsive genes and transcription factors were identified within the flanking region of differential peaks. When drought was compared to control, it showed upregulated differential peaks primarily in the promoter and distal intergenic regions. Conclusion: By analyzing FAIRE we are able to identify distinct genomic regions corresponding to droughts and controls. Upstream regions of genes play a significant role in drought stress response. Our data suggest that promoter regions of >2 kb, downstream regions of <= 300, and distant regulatory regions are predominant during the upregulation of drought stress. It would also be helpful to note that genomic regions vary in response to drought, and distal intergenic regions may also be involved in drought responses. Understanding plant genomes and epigenomics could help us develop varieties that can withstand extreme weather conditions.
2023-11-08 | GSE187025 | GEO
Project description:Melanoma genomes are often characterized by large numbers of sunlight-induced mutations. However, epigenetic alterations, in the form of aberrant DNA methylation patterns, are also abundant. Using MIRA-seq, we have carried out a comprehensive characterization of the DNA methylome in a series of metastatic melanoma samples and catalogued the methylation changes relative to normal melanocytes, the presumed cells of origin for these tumors. Individual melanoma tumors contained up to several thousand hypermethylated regions. We discovered 179 tumor-specific methylation peaks that were present in all (27/27) melanomas and may lend themselves as effective disease biomarkers, and 3124 methylation peaks were present in >40% of the tumors. We specifically examined the relationship between presence of the Polycomb mark, H3K27me3 in melanocytes and tumor-specific DNA methylation in melanoma. We found that 150 of the approximately 1,200 tumor-associated methylation peaks near transcription start sites (TSS) were H3K27me3-marked in melanocytes. Notably, DNA methylation in melanoma was specific for distinct H3K27me3 peaks rather than for H3K27me3-enriched regions with broad genomic coverage. Yet, there were also numerous H3K27me3 peak-associated TSS regions that were completely resistant to DNA methylation in tumors. Furthermore, a rather large group of genes became methylated in melanoma but lacked H3K27me3 in melanocytes. There was no relationship between presence of BRAF V600 mutations and the number of methylation peaks in individual tumors. Gene expression analysis showed a strong signature of upregulated immune response genes in melanomas presumably as a result of lymphocyte infiltration. Genes down-regulated in tumors were enriched for melanocyte differentiation and pigmentation factors. Overall, there was limited correlation between tumor-associated DNA methylation changes and changes in gene expression although distinct melanocyte differentiation genes including KIT, PAX3 and SOX10 became methylated and downregulated in melanoma. Examination of H3K27me3 histone modification in human normal melanocytes.
2016-03-31 | E-GEOD-71692 | biostudies-arrayexpress
Project description:Melanoma genomes are often characterized by large numbers of sunlight-induced mutations. However, epigenetic alterations, in the form of aberrant DNA methylation patterns, are also abundant. Using MIRA-seq, we have carried out a comprehensive characterization of the DNA methylome in a series of metastatic melanoma samples and catalogued the methylation changes relative to normal melanocytes, the presumed cells of origin for these tumors. Individual melanoma tumors contained up to several thousand hypermethylated regions. We discovered 179 tumor-specific methylation peaks that were present in all (27/27) melanomas and may lend themselves as effective disease biomarkers, and 3124 methylation peaks were present in >40% of the tumors. We specifically examined the relationship between presence of the Polycomb mark, H3K27me3 in melanocytes and tumor-specific DNA methylation in melanoma. We found that 150 of the approximately 1,200 tumor-associated methylation peaks near transcription start sites (TSS) were H3K27me3-marked in melanocytes. Notably, DNA methylation in melanoma was specific for distinct H3K27me3 peaks rather than for H3K27me3-enriched regions with broad genomic coverage. Yet, there were also numerous H3K27me3 peak-associated TSS regions that were completely resistant to DNA methylation in tumors. Furthermore, a rather large group of genes became methylated in melanoma but lacked H3K27me3 in melanocytes. There was no relationship between presence of BRAF V600 mutations and the number of methylation peaks in individual tumors. Gene expression analysis showed a strong signature of upregulated immune response genes in melanomas presumably as a result of lymphocyte infiltration. Genes down-regulated in tumors were enriched for melanocyte differentiation and pigmentation factors. Overall, there was limited correlation between tumor-associated DNA methylation changes and changes in gene expression although distinct melanocyte differentiation genes including KIT, PAX3 and SOX10 became methylated and downregulated in melanoma. Genome-wide gene expression analysis of 17 melanomas and 3 melanocyte samples
2016-03-31 | E-GEOD-71747 | biostudies-arrayexpress
Project description:Melanoma genomes are often characterized by large numbers of sunlight-induced mutations. However, epigenetic alterations, in the form of aberrant DNA methylation patterns, are also abundant. Using MIRA-seq, we have carried out a comprehensive characterization of the DNA methylome in a series of metastatic melanoma samples and catalogued the methylation changes relative to normal melanocytes, the presumed cells of origin for these tumors. Individual melanoma tumors contained up to several thousand hypermethylated regions. We discovered 179 tumor-specific methylation peaks that were present in all (27/27) melanomas and may lend themselves as effective disease biomarkers, and 3124 methylation peaks were present in >40% of the tumors. We specifically examined the relationship between presence of the Polycomb mark, H3K27me3 in melanocytes and tumor-specific DNA methylation in melanoma. We found that 150 of the approximately 1,200 tumor-associated methylation peaks near transcription start sites (TSS) were H3K27me3-marked in melanocytes. Notably, DNA methylation in melanoma was specific for distinct H3K27me3 peaks rather than for H3K27me3-enriched regions with broad genomic coverage. Yet, there were also numerous H3K27me3 peak-associated TSS regions that were completely resistant to DNA methylation in tumors. Furthermore, a rather large group of genes became methylated in melanoma but lacked H3K27me3 in melanocytes. There was no relationship between presence of BRAF V600 mutations and the number of methylation peaks in individual tumors. Gene expression analysis showed a strong signature of upregulated immune response genes in melanomas presumably as a result of lymphocyte infiltration. Genes down-regulated in tumors were enriched for melanocyte differentiation and pigmentation factors. Overall, there was limited correlation between tumor-associated DNA methylation changes and changes in gene expression although distinct melanocyte differentiation genes including KIT, PAX3 and SOX10 became methylated and downregulated in melanoma. Using MIRA-Seq, DNA methylation profiles of 27 malignant melanomas and 3 primary cultured melanocyte samples were determined
2016-03-31 | E-GEOD-71938 | biostudies-arrayexpress
Project description:Purpose: We used ChIP-seq to analyze daily transcription and regulation of Pol II pausing within the mouse liver. Methods: Livers of young mice were processed for Pol II and Nelf-A ChIP-seq at 4-h interval across the day. The binding pattern was analyzed by MACS. Tag pileup within promoter and gene body regions were also obtained to calculate Pol II TR. Results: We obtained > 10 million high quality sequencing reads per time points per sample after quality control and alignments. MACS identified nearly 10,000 Pol II peaks genomewide throughout the day. Nelf-A peaks varied from a few hundreds to 10,000 across the day. A genomewide Nelf-A binding rhythm was evident. We also quantitated bindings within the TSS region and/or gene body and analyzed the quantitation results with ARSER for rhythm detection. We found Pol II binding within the TSS region and gene body show discordant changes. While most genes had peak TSS Pol II binding around dawn, Pol II binding within the gene body showed more scattered distribution, with two peaks around dawn and dusk, respectively. Pol II traveling ratio also showed daily changes, with most genes having a higher TR around dawn. Conclusions: Our study revealed discordant Pol II rhythms in the TSS region and within the gene body, and indicated that Pol II initiation and pause release could have distinct roles in the generation of transcription rhythms within the mouse liver.
2018-12-20 | GSE96773 | GEO
Project description:We investigate the transcriptome response of porcine intestinal epitheliocyte cell line (PIE cells) to the challenge with heat-stable Enterotoxigenic Escherichia coli (ETEC) pathogen-associated molecular patterns (PAMPs) and, the changes induced by Lactobacillus jensenii TL2937 in that response. The transcriptome approach allowed us to obtain a global overview of the immune and immune related genes involved in response of PIE cells to heat-stable ETEC PAMPs. The most remarkable changes in PIE cells after heat-stable ETEC PAMPs challenge were observed in chemokines expressions, followed by cell adhesion molecules and, complement and coagulation cascades factors. We also confirmed that L. jensenii TL2937 differently modulates gene expression in ETEC PAMPs-challenged PIE cells. The microarray gene expression profiles clearly demonstrated that an anti-inflammatory effect was triggered by the immunobiotic strain in PIE cells. The main outcome from the study was the differential regulation of chemokines (CCL8, CXCL5, CXCL9, CXCL10 and CXCL11), complement factors (C1R, C1S, C3 and CFB) and, coagulation system proteins (Tissue factor) expression by L. jensenii TL2937. PIE cells treated with the negative control Lactobacillus plantarum TL2766 showed a transcriptomic response similar to ETEC PAMPs-challenged PIE cells.
2016-01-22 | GSE77095 | GEO
Project description:We found that radiation treatment enhanced the expression of H3K27me3 in glioblastoma. Thus, we asked whether radiation contributed to the increase of global genomic H3K27me3 occupancy in glioblastoma. The Chip-seq results in GL261 cells showed that irradiation led to the increase of H3K27me3 occupancy ±50kb within the transcription start sites (TSS), especially the promoter sites (peaks±2kb within TSS). Some pathways, in which H3K27me3 peaks significantly enriched, were found. Chip-seq was conducted for H3K27me3 in glioblastoma cell line GL261 when GL261 cells were treated with or without irradiation.
2022-06-01 | GSE205062 | GEO
Project description:Purpose: Define the chromatin remodelling induced by second generation HDACIs Outcome: We demonstrate that NKL54 treatment increased the number of H3K27ac peaks and caused a slight redistribution of H3K27ac peaks in promotorial regions. The hyperacetylation effect is evident in poorly acetylated loci, while hyperacetylated TSS turned out to be paradoxically deacetylated by NKL54 treatment. NKL54 caused a reduction in the binding of HDAC4 and HDAC9, especially at the intergenic regions. Instead, their binding to promoters was conserved. In contrast, NKL54 caused a dramatic increase in MEF2D binding to several genomic regions and especially to promoters. These new NKL54-enhanced MEF2D-chromatin interactions are often located at new genomic regions, whereas 40% of MEF2D peaks in untreated cells are conserved in NKL54-treated cells. Importantly, in these new regions, MEF2D is frequently recruited in the absence of HDAC4 or of HDAC9.
2022-01-25 | GSE180681 | GEO
Project description:Loss of CLP1 activity results in the accumulation of novel sets of small RNA fragments derived from aberrant processing of tyrosine pre-tRNA. Such tRNA fragments sensitize cells to oxidative stress-induced p53 activation and p53-dependent cell death.
2013-04-03 | GSE39275 | GEO
Project description:Melanoma genomes are often characterized by large numbers of sunlight-induced mutations. However, epigenetic alterations, in the form of aberrant DNA methylation patterns, are also abundant. Using MIRA-seq, we have carried out a comprehensive characterization of the DNA methylome in a series of metastatic melanoma samples and catalogued the methylation changes relative to normal melanocytes, the presumed cells of origin for these tumors. Individual melanoma tumors contained up to several thousand hypermethylated regions. We discovered 179 tumor-specific methylation peaks that were present in all (27/27) melanomas and may lend themselves as effective disease biomarkers, and 3124 methylation peaks were present in >40% of the tumors. We specifically examined the relationship between presence of the Polycomb mark, H3K27me3 in melanocytes and tumor-specific DNA methylation in melanoma. We found that 150 of the approximately 1,200 tumor-associated methylation peaks near transcription start sites (TSS) were H3K27me3-marked in melanocytes. Notably, DNA methylation in melanoma was specific for distinct H3K27me3 peaks rather than for H3K27me3-enriched regions with broad genomic coverage. Yet, there were also numerous H3K27me3 peak-associated TSS regions that were completely resistant to DNA methylation in tumors. Furthermore, a rather large group of genes became methylated in melanoma but lacked H3K27me3 in melanocytes. There was no relationship between presence of BRAF V600 mutations and the number of methylation peaks in individual tumors. Gene expression analysis showed a strong signature of upregulated immune response genes in melanomas presumably as a result of lymphocyte infiltration. Genes down-regulated in tumors were enriched for melanocyte differentiation and pigmentation factors. Overall, there was limited correlation between tumor-associated DNA methylation changes and changes in gene expression although distinct melanocyte differentiation genes including KIT, PAX3 and SOX10 became methylated and downregulated in melanoma.
2016-03-31 | GSE71938 | GEO