Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA243850 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1220080.fastq.gz | Fastqsanger.gz | |||
| SRR1220081.fastq.gz | Fastqsanger.gz | |||
| SRR1220082.fastq.gz | Fastqsanger.gz | |||
| SRR1220083.fastq.gz | Fastqsanger.gz | |||
| SRR1220084.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 7 |
Similar Datasets
Project description:Impact of human MLL/COMPASS and Polycomb complexes on the DNA methylome [expression array]
| PRJNA243852 | ENA
Project description:The transcriptional activating and repressive functions performed by Trithorax and Polycomb group complexes, respectively, are critical for to maintain cellular fates in ontogeny and in cancer. Here we report that leukemias initiated by a Trithorax-related oncogene, MLL-AF9, depend upon the Polycomb Repressive Complex 2 (PRC2) to sustain a transformed cellular state. RNAi mediated suppression of PRC2 subunits is sufficient to inhibit proliferation of MLL-AF9 leukemias, with little impact on growth of non-transformed cells. This requirement is partly due to PRC2-mediated transcriptional repression of several anti-self-renewal regulators, including Cdkn2a. These results suggest that, unlike the classical antagonism generally observed between Polycomb and Trithorax group proteins during development, the activities of these two pathways can cooperate to promote myeloid neoplasia. In order to understand downstream targets of PRC2 complex in MLL-AF9 leukemia, we performed array in murine MLL-AF9/NrasG12D cell line under the condition that two subunits of PRC2(Eed and Suz12) were suppressed by using shRNAs.
2013-07-01 | E-GEOD-34183 | biostudies-arrayexpress
Project description:Elevated plasma homocysteine is an independent risk factor for cardiovascular disease and stroke, however the etiology remains poorly understood. Elevated homocysteine is known to inhibit methyltransferases including DNA methyltransferases, but no methylome-wide analysis of elevated homocysteine has been reported. Peripheral blood genomic DNA methylation in 8 Singaporean-Chinese ischemic stroke patients (4 male, 4 female) with varying homocysteine titer and hypertensive status were profiled using methyl-CpG binding domain (MBD) protein-enriched genome sequencing (MBD-seq) on Illumina Genome Analyzer IIx. A methylome wide screen was undertaken for gender, total plasma homocysteine, hypertension and age. The data show considerable variability within the small cohort, including at genes which are related to one carbon metabolism and cardiovascular disease. Peripheral blood genomic DNA methylation in 8 Singaporean-Chinese ischemic stroke patients (4 male, 4 female) was profiled using methyl-CpG binding domain (MBD) protein-enriched genome sequencing (MBD-seq) on Illumina Genome Analyzer IIx. Methylation parrterns were correlated with homocysteine levels, lypertensive status, gender and age.
2014-05-27 | E-GEOD-57962 | biostudies-arrayexpress
Project description:COMPASS and Polycomb complexes are antagonistic chromatin complexes that are frequently inactivated in cancers, but how their inactivation affects the cellular hierarchy, composition and growth of tumors is unclear. Such characteristics can be systematically investigated in Drosophila neuroblast tumors in which cooption of temporal patterning induces a developmental hierarchy that confers cancer stem cell (CSC) properties to a subset of neuroblasts retaining an early larval temporal identity. Here, using single-cell transcriptomics, we reveal that the trithorax/MLL1/2-COMPASS-like complex guides the developmental trajectory at the top of the tumor hierarchy. Consequently, trithorax inactivation drives larval-to-embryonic temporal reversion and the dramatic expansion of CSCs that remain locked in a spectrum of early temporal states. Surprisingly, this phenotype is amplified by concomitant inactivation of Polycomb Repressive Complex 2 genes, unleashing tumor growth. This study exemplifies how inactivation of specific COMPASS and Polycomb complexes cooperates to impair tumor hierarchies and induce CSC plasticity and heterogeneity.
2021-08-31 | GSE179154 | GEO
Project description:Methylation of lysine 4 at histone H3 (H3K4) at promoters is tightly linked to transcriptional regulation in human cells. At least six different COMPASS-like multi-subunit (SET1/MLL) complexes have been described that contain methyltransferase activity towards H3K4, but a comprehensive and quantitative analysis of these SET1/MLL complexes is lacking. We applied label-free quantitative mass spectrometry to determine the subunit composition and stoichiometry of the human SET1/MLL complexes. Peptides were applied to online nanoLC-MS/MS, using a 120 min acetonitrile gradient (5.6 - 76%). Mass spectra were recorded on an LTQ-Orbitrap-Velos mass spectrometer (Thermo) selecting the 15 most intense precursor ions of every full scan for fragmentation. Raw data were analyzed using MaxQuant 1.3.0.5, with label-free quantification (LFQ), match between runs (between triplicates) and the iBAQ algorithm enabled. MaxQuant default settings were used for peptide identification; Enzyme: Trypsin/P, MS tolerance (FTMS): 6 ppm, max missed cleavages: 2, max charge: 7, MS/MS tolerance (ITMS): 0.5 Da, Peptide FDR: 0.01 and Protein FDR: 0.01. Normalized mass spectrometric intensities (LFQ intensities) were compared between the GFP-tagged and control sample, using an adapted permutation-based false discovery rate (FDR) t-test in Perseus (MaxQuant package).
2013-09-13 | PXD000172 | Pride
Project description:The transcriptional activating and repressive functions performed by Trithorax and Polycomb group complexes, respectively, are critical for to maintain cellular fates in ontogeny and in cancer. Here we report that leukemias initiated by a Trithorax-related oncogene, MLL-AF9, depend upon the Polycomb Repressive Complex 2 (PRC2) to sustain a transformed cellular state. RNAi mediated suppression of PRC2 subunits is sufficient to inhibit proliferation of MLL-AF9 leukemias, with little impact on growth of non-transformed cells. This requirement is partly due to PRC2-mediated transcriptional repression of several anti-self-renewal regulators, including Cdkn2a. These results suggest that, unlike the classical antagonism generally observed between Polycomb and Trithorax group proteins during development, the activities of these two pathways can cooperate to promote myeloid neoplasia.
2013-07-01 | GSE34183 | GEO
Project description:We studied the effects of chemical exposure on global DNA methylation by using mCherry-methyl-CpG-binding domain (MBD)-nls human induced pluripotent stem cells (iPSCs). According to the fluorescent MBD parameters, we divided the effects of 135 chemical on global DNA methylation into 3 categories; reduction (hypomethylation), increase (hypermethylation) and little/no effect. We performed DNA methylome assay to examine the effects of 6 epigenotoxic chemicals on genome-wide DNA methylation patterns in human iPSCs. Our results indicated that hypermethylation agents increased DNA methylation and downregulated the expression of genes involved in cell cycle or development.
2021-07-23 | GSE180453 | GEO
Project description:The evolutionally conserved COMPASS complexes are responsible for the catalyzation of H3K4 methylations. Recently, three types of COMPASS complexes which contains histone methyltransferases ATX1/2, ATX3, or ATX4/5 were identified in Arabidopsis. Here, we report the ATX proteins are essential for the survival of Arabidopsis. By RNA-seq and chromatin immunoprecipitation (ChIP-seq) analysis, we found ATX1/2-, ATX3-, and ATX4/5-containing COMPASS complex redundantly regulate gene expression and H3K4me3 modifications. In addition to the developmental-related genes, we found the expression of DNA methylation-related genes were also regulated by the COMPASS complexes. The transcript and H3K4me3 levels at the RdDM pathway genes (NRPE1, DCL3, IDN2, FDM2) and at the DNA demethylase encoding genes (ROS1, DML2, DML3) were down-regulated in atx1/2/4/5 mutants. Via bisulfate sequencing, we found the atx1/2/4/5 showed hypermethylation at CG and CHG contexts whereas the hypomethylation at CHH contexts. By comparing the differentially methylated regions (DMRs) in atx1/2/4/5 with that in ros1;dml2;dml3 (rdd) and in nrpe1, a large part of overlapping DMRs were identified. Based on these results and other findings, we propose that the hypermethylation in CG and CHG is partially caused by the down-regulation of ROS1/DML2/DML3, and the hypomethylation in CHH is mainly caused by the down-regulation of NRPE1. Furthermore, we revealed that the COMPASS complexes also play a redundant role in regulating the transcription of transposable elements (TEs). This study extends our knowledge about the function of COMPASS in plant development and illustrate the important roles for COMPASS complexes in the regulation of DNA methylation and TEs transcription.
2022-11-14 | GSE206687 | GEO
Project description:The evolutionally conserved COMPASS complexes are responsible for the catalyzation of H3K4 methylations. Recently, three types of COMPASS complexes which contains histone methyltransferases ATX1/2, ATX3, or ATX4/5 were identified in Arabidopsis. Here, we report the ATX proteins are essential for the survival of Arabidopsis. By RNA-seq and chromatin immunoprecipitation (ChIP-seq) analysis, we found ATX1/2-, ATX3-, and ATX4/5-containing COMPASS complex redundantly regulate gene expression and H3K4me3 modifications. In addition to the developmental-related genes, we found the expression of DNA methylation-related genes were also regulated by the COMPASS complexes. The transcript and H3K4me3 levels at the RdDM pathway genes (NRPE1, DCL3, IDN2, FDM2) and at the DNA demethylase encoding genes (ROS1, DML2, DML3) were down-regulated in atx1/2/4/5 mutants. Via bisulfate sequencing, we found the atx1/2/4/5 showed hypermethylation at CG and CHG contexts whereas the hypomethylation at CHH contexts. By comparing the differentially methylated regions (DMRs) in atx1/2/4/5 with that in ros1;dml2;dml3 (rdd) and in nrpe1, a large part of overlapping DMRs were identified. Based on these results and other findings, we propose that the hypermethylation in CG and CHG is partially caused by the down-regulation of ROS1/DML2/DML3, and the hypomethylation in CHH is mainly caused by the down-regulation of NRPE1. Furthermore, we revealed that the COMPASS complexes also play a redundant role in regulating the transcription of transposable elements (TEs). This study extends our knowledge about the function of COMPASS in plant development and illustrate the important roles for COMPASS complexes in the regulation of DNA methylation and TEs transcription.
2022-11-14 | GSE206685 | GEO