ATAC-seq analysis of radioresistant/sensitive cells in oral cancer
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE180074 | GEO | 2022/01/01
REPOSITORIES: GEO
Similar Datasets
Project description:In this study, we used ATAC sequencing to compare the chromatin landscape of esophageal cells in which hedgehog (HH) pathway has been activated (K5SmoM2), to control esophageal cells (WT). We identified more than 50% of the peaks differentially opened in both conditions. Among these differentially opened peaks in EpHI cells, we identified chromatin regions in key columnar markers. Taken together these results show that HH pathway activation triggers chromatin landscape remodeling to facilitate transcommitment.
2021-04-20 | GSE148872 | GEO
Project description:Hematopoietic stem cells (HSCs) react to various stress conditions. However, it is unclear whether and how HSCs respond to severe anemia. Here, we demonstrate that upon induction of acute anemia, HSCs rapidly proliferate and enhance their erythroid differentiation potential. In severe anemia, lipoprotein profiles largely change and the concentration of ApoE increases. In HSCs, transcription levels of lipid metabolism-related genes, such as very low-density lipoprotein receptor (Vldlr), are upregulated. Stimulation of HSCs with ApoE enhances their erythroid potential, whereas HSCs in Apoe knockout mice do not respond to anemia induction. VldlrhighHSCs show higher erythroid potential, which is enhanced after acute anemia induction. VldlrhighHSCs are epigenetically distinct because of their low chromatin accessibility, and more chromatin regions are closed upon acute anemia induction. Chromatin regions closed upon acute anemia induction are mainly binding sites of Erg. Inhibition of Erg enhanced the erythroid differentiation potential of HSCs. Our findings indicate that lipoprotein metabolism plays a crucial role in HSC regulation under severe anemic conditions.
2024-08-07 | GSE274144 | GEO
Project description:Background: Growth hormone-secreting pituitary adenoma (GHPA) is an insidious disease with persistent hypersecretion of growth hormone and insulin-like growth factor 1, leading to increased morbidity and mortality. Though treatments for GHPA have greatly improved, lack of deep knowledge on the precise molecular mechanisms involved in GHPA hinders the development of therapeutic approaches. Few studies have attempted to reveal the genome-wide landscape of GHPA. As chromatin structure change exerts significant influence on gene transcription, herein, we investigated the landscape of chromatin accessibility. Methods: Both assay for transposase-accessible chromatin with high-throughput sequencing (ATAC-seq) and RNA sequencing (RNA-seq) were applied to identify the differential expression genes (DEGs) and uncover chromatin accessibility changes and the potentially associated transcription factor (TFs) in somatotropinoma tissues. Results: 64 DEGs were obtained, including 10 DEGs were elevated in the tumors and 54 DEGs were negligibly expressed in adenomas. A total of 3916 increased and 2895 decreased chromatin-accessible regions were identified nearby these DEGs. The majority of DEGs associated with closed chromatin regions were significantly down-regulated in our study, while the most of DEGs near open chromatin were not expectantly up-regulated. Additionally, the newly opened and closed chromatin regions were highly enriched for GRE and CTCF transcription factor binding sites, which were potentially relevant to the regulation of chromatin accessibility and genes expression in GHPA. Conclusion: Collectively, our results reveal the landscape of chromatin accessibility and unique enhancer in GHPA, which may, at least in part, contribute to tumorigenesis and provide a new field of drug development.
2021-08-18 | GSE182180 | GEO
Project description:Adult hematopoietic stem cells (HSCs) react to various stress conditions by rapidly proliferating and preferentially differentiating towards desired cell types. However, it is unclear whether and how HSCs respond to severe anemic conditions. Here we demonstrate that HSCs rapidly proliferate and enhance their erythroid potential upon induction of acute anemia. Under severe anemic conditions, the concentration of erythropoietin (EPO) does not increase in the bone marrow. Instead, lipoprotein profiles largely changed, and the concentration of apolipoprotein E (ApoE) increased. In HSCs, transcription levels of lipid metabolism-related genes such as very low-density lipoprotein receptor (Vldlr) were significantly up-regulated. Stimulation of HSCs with recombinant ApoE enhanced the erythroid potential, while HSCs of ApoE knockout mice did not respond to the hemolysis induction. We also found that VLDLRhighHSCs have higher erythroid differentiation potential, particularly after acute anemia induction. VLDLRhighHSCs were epigenetically distinct from VLDLRlowHSCs, as their chromatin accessibility was lower and more chromatin regions were closed upon acute anemia induction. Finally, we identified that the chromatin regions closed upon the acute anemia induction were mainly binding sites of a transcription factor Erg. Treatment of HSC with Erg inhibitor enhanced erythroid differentiation potential, as seen in the ApoE treatment. Our findings indicate that lipoprotein metabolism, particularly ApoE, plays a crucial role in HSC regulation under severe anemia conditions in a non-canonical fashion, unlike a conventional factor such as EPO.
2023-06-30 | GSE212392 | GEO
Project description:MOM1 is an Arabidopsis factor previously shown to mediate transcriptional silencing independent of major DNA methylation changes. Here we found that MOM1 localizes with sites of RNA-directed DNA methylation (RdDM). Tethering MOM1 with artificial zinc finger to unmethylated FWA promoter led to establishment of DNA methylation and FWA silencing. This process was blocked by mutations in components of the Pol V arm of the RdDM machinery, as well as by mutation of MORC6. We found that at some endogenous RdDM sites, MOM1 is required to maintain DNA methylation and a closed chromatin state. In addition, efficient silencing of newly introduced FWA transgenes was impaired by mutation of MOM1 or mutation of genes encoding the MOM1 interacting PIAL1/2 proteins. In addition to RdDM sites, we identified a group of MOM1 peaks at active chromatin near genes that colocalized with MORC6. These findings demonstrate a multifaceted role of MOM1 in genome regulation.
2023-06-10 | PXD039991 | Pride
Project description:We report epigenetic changes in the chromatin accessibility landscape of retinal myeloid cells from mice preconditioned with 4xLPS injections persist after the initial inflammation has subsided. We compared the data of scATAC-seq performed on nuclei extracted from sorted CX3CR1+ retinal cells from mice 3 days after CNV induction, preconditioned with either PBS or 4xLPS 1 month before, or Naïve retinas without CNV induction, preconditioned with PBS. After quality control, filtering and dimension reduction, a two-dimensional UMAP was performed on the remaining 835, 821, and 588 cells in the PBS, 4xLPS, and Naive groups respectively. Unbiased clustering was applied using Leiden algorithm, which partitioned CX3CR1+ myeloid cells into 8 distinct clusters (C1–C8). Based on previously described cell-specific gene signatures, we identified microglia (clusters C1, C2 and C3), monocytes (clusters C4 and C5), and macrophages (cluster C6). Gene expression scores identified C4 as circulating monocytes and C5 as a mixture of classical and inflammatory monocytes. The three microglial populations (C1, C2, and C3), harbor the greatest epigenetic diversity following induction of CNV or preconditioning. GSEA analysis revealed that the C2 subpopulation was characterized by considerable enrichment in opened chromatin regions corresponding to genes coding for inflammation-related pathways. In contrast, the C1 subpopulation showed higher numbers of closed chromatin in genes coding for inflammatory processes. Moreover, when compared to the C1 and C2 subpopulations, C3 had open chromatin regions only in two gene sets coding for inflammation-related pathways, and three gene sets with closed chromatin regions. Together, these data demonstrate that the chromatin landscape of retina-resident microglia is impacted differently by both the prior systemic exposure to LPS and by CNV.
2023-02-22 | GSE194226 | GEO
Project description:We have studied the impact of T2D on open chromatin in human pancreatic islets. We used assay for transposase-accessible chromatin using sequencing (ATAC-seq) to profile open chromatin in islets from T2D and non-diabetic donors. We identified ATAC-seq peaks representing open chromatin regions in islets of non-diabetic and diabetic donors. The majority of ATAC-seq peaks mapped near transcription start sites. Additionally, peaks were enriched in enhancer regions and in regions where islet-specific TFs bind. Islet ATAC-seq peaks overlap with SNPs associated with T2D and with additional SNPs in LD with known T2D SNPs. There was enrichment of open chromatin regions near highly expressed genes in human islets.
2019-04-06 | GSE129383 | GEO
Project description:Purpose: Evaluate changes in chromatin accessibility between human embryonic stem cells and surface ectoderm cells with and without the transcription factor p63. Method: Chromatin accessibility profiles for human embryonic stem cells and surface ectoderm with and without p63 were generated by deep sequencing, in duplicate, with the Illumina NextSeq sequencer. Quality reads were assessed by fastq. Reads were aligned using Bowtie2, PCR duplicates and mitochondrial DNA were discarded, and peak calling was completed using MACS2. Non-reproducible peaks were filtered out by IDR with an FDR of 5%. Results: p63 fails to modify chromatin accessibility when ectopically expressed in human embryonic stem cells; differentiation of human embryonic stem cells to surface ectoderm results in the closure of some regions open in pluripotent cells and the opening of new regions; and loss of p63 in the surface ectoderm results in increased accessibility of 1/3 of the regions opened during surface ectoderm differentiation. Conclusion: p63's ability to modify chromatin accessibility is dependent upon the underlying epigenetic landscape, and when it can modify the landscape, it does so by closing regions that become open during ectoderm differentiation.
2018-11-06 | GSE119996 | GEO
Project description:Escherichia coli strain:1929 | isolate:1929 Genome sequencing
| PRJNA295348 | ENA
Project description:Stomata are pores in the epidermis of plants that can open and close, allowing for gas exchange with the environment, vital for photosynthesis, and regulating transpiration. They are formed from protodermal cells by a series of asymmetric and symmetric divisions and differentiation steps. Initiation into and progression within the stomatal lineage are driven by the consecutive expression and action of three sets of bHLH transcription factor dimers (SPCH, MUTE, FAMA plus their heterodimer partners SCRM or SCRM2) and is accompanied by massive changes in the transcriptome as well as the chromatin landscape. Strong shifts in chromatin accessibility have been observed specifically at the initiation stage and at the transition from division to differentiation. In line with this, FAMA, which promotes the differentiation of stomata, has been shown to interact with RBR, which can recruit the repressive PRC2 complex, to shut down the early stomatal lineage transcriptional program. Interestingly, several of the stomatal lineage bHLHs bind chromatin regions that are closed/inaccessible in a primordial state (the shoot apical meristem). This suggests that the stomatal lineage bHLHs could be able to access closed chromatin and that they might also be directly involved in opening (and closing) of chromatin at a subset of their target regions. In order to test this hypothesis and identify chromatin modifiers that associate with the stomatal lineage bHLH dimers, we did proximity labeling with TurboID fused to SCRM, which is expressed throughout the stomatal lineage and is the main heterodimerization partner of SPCH, MUTE and FAMA. We identified a number of proteins acting as chromatin modifiers and remodelers, including the histone acetyl transferase HAC1, which deposits activating marks on nucleosomes, and multiple subunits of the ATPase-dependent chromatin remodeling SWI/SNF complex. Together, these data support a role of SCRM and its partners in regulating target gene accessibility to impose lasting changes in gene expression within the stomatal lineage.
2024-06-14 | PXD040690 | Pride