Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-42212E-MEXP-3776E-MEXP-3778E-MEXP-3777
PROVIDER: PRJNA179295 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR616131.fastq.gz | Fastqsanger.gz | |||
| SRR616132.fastq.gz | Fastqsanger.gz | |||
| SRR616133.fastq.gz | Fastqsanger.gz | |||
| SRR616134.fastq.gz | Fastqsanger.gz | |||
| SRR616135.fastq.gz | Fastqsanger.gz |
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Project description:Human epidermal stem cells transit from a slow cycling to an actively proliferating state to contribute to homeostasis. Both stem cell states differ in their cell cycle profiles but must remain guarded from differentiation and senescence. Here we show that Cbx4, a Polycomb Repressive Complex-1 (PRC1)-associated protein, maintains human epidermal stem cells slow-cycling and undifferentiated, while protecting them from senescence. Interestingly, abrogating the polycomb activity of Cbx4 impairs its anti-senescent function without affecting stem cell differentiation, indicating that differentiation and senescence are independent processes in human epidermis. Conversely, Cbx4 inhibits stem cell activation and differentiation through its SUMO ligase activity. Global transcriptome and chromatin occupancy analyses indicate that Cbx4 regulates modulators of epidermal homeostasis and represses factors, such as Ezh2, Dnmt1, and Bmi1, to prevent the activate stem cell state. Our results suggest that distinct Polycomb complexes balance epidermal stem cell dormancy and activation, while continually preventing senescence and differentiation. Primary human keratinocytes were infected with control vector pBABE, Cbx4 wildtype and a Sumoylation mutant version of Cbx4 (the two Sumo Interaction Motifs were deleted), both fused to a Estrogen Receptor to render their activaty inducible by addition of 4OHT to the media. Cells were cultured for 5 days (after infection and selection) under 4OHT treatment, after which total RNA was collected.
2011-08-01 | E-GEOD-31094 | biostudies-arrayexpress
Project description:CARM1 is an integral component of the NuRD chromatin remodeling complex
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Project description:CARM1 is an integral component of the NuRD chromatin remodeling complex
| PRJNA545133 | ENA
Project description:In addition to the glucocorticoids, the glucocorticoid receptor (GR) is regulated by post-translational modifications, including SUMOylation. We have analyzed how SUMOylation influences the activity of endogenous GR target genes and the receptor chromatin binding by using isogenic HEK293 cells expressing wild-type GR (wtGR) or SUMOylation-defective GR (GR3KR). Gene expression profiling revealed that both dexamethasone up- and down-regulated genes are affected by the GR sumoylation and that the affected genes are significantly associated with pathways of cellular proliferation and survival. The GR3KR-expressing cells proliferated more rapidly and their anti-proliferative response to dexamethasone was less pronounced than in the wtGR-expressing cells. ChIP-seq analyses indicated that the SUMOylation modulates the chromatin occupancy of GR on several loci associated with cellular growth in a fashion which parallels with their differential dexamethasone-regulated expression between the two cell lines. Moreover, genome-wide SUMO-2/3 marks, which were generally associated with active chromatin, showed markedly higher overlap with the wtGR cistrome than with the GR3KR cistrome. In sum, our results indicate that the SUMOylation does not simply repress the GR activity, but regulates the activity of the receptor in a target locus selective fashion, playing an important role in controlling the GR activity on genes influencing cell growth. Examination of GR and SUMO-2/3 binding from isogenic HEK293 cell lines stably expressing either wtGR or GR3KR, in biological duplicates, using Illumina HiSeq 2000. GR binding from control HEK293 (FRT) cell line and input sample from FRT were used as controls for GR. Sequenced IgG sample from FRT cell line was used as control for SUMO-2/3
2013-11-05 | E-GEOD-48374 | biostudies-arrayexpress
Project description:Glucocorticoids (GCs) are a crucial component of effective treatment for acute lymphoblastic leukemia (ALL). GCs exert their functions through the glucocorticoid receptor (GR), a ligand-activated transcription factor (TF). Chromatin occupancy, chromatin-protein networks and gene programmes of GR are regulated by SUMOylation, which has therapeutic implications in other hematomalignancies. To unravel the GR-SUMO crosstalk in ALL, we induced a hypoSUMOylated state in NALM6 ALL cells with a SUMOylation inhibitor (ML-792). Genome-wide profiling of GR and SUMO binding and chromatin accessibility revealed that hypoSUMOylation augmented GR chromatin occupancy and altered chromatin openness upon dexamethasone (Dex) exposure. Association with transcriptome data indicated that on the novel binding sites GR predominantly suppressed target gene expression. Chromatin-proteomic analyses identified a substantial number of shared TFs and coregulators associated with chromatin-bound GR and SUMO. The chromatin-protein network of GR contained several TFs with corresponding binding motifs found on GR-adjacent chromatin sites, implying their simultaneous presence on chromatin. Cell cycle and proliferation analyses indicated that hypoSUMOylation potentiated Dex-induced cell cycle arrest and suppressed NALM6 cell proliferation, complementing the significant expression changes of cell cycle-related genes in our transcriptome data. Our work provides a valuable resource of GR chromatin partners and implies potential for targeting SUMOylation to increase sensitivity to GCs in ALL.
2025-01-20 | GSE233551 | GEO
Project description:Glucocorticoids (GCs) are a crucial component of effective treatment for acute lymphoblastic leukemia (ALL). GCs exert their functions through the glucocorticoid receptor (GR), a ligand-activated transcription factor (TF). Chromatin occupancy, chromatin-protein networks and gene programmes of GR are regulated by SUMOylation, which has therapeutic implications in other hematomalignancies. To unravel the GR-SUMO crosstalk in ALL, we induced a hypoSUMOylated state in NALM6 ALL cells with a SUMOylation inhibitor (ML-792). Genome-wide profiling of GR and SUMO binding and chromatin accessibility revealed that hypoSUMOylation augmented GR chromatin occupancy and altered chromatin openness upon dexamethasone (Dex) exposure. Association with transcriptome data indicated that on the novel binding sites GR predominantly suppressed target gene expression. Chromatin-proteomic analyses identified a substantial number of shared TFs and coregulators associated with chromatin-bound GR and SUMO. The chromatin-protein network of GR contained several TFs with corresponding binding motifs found on GR-adjacent chromatin sites, implying their simultaneous presence on chromatin. Cell cycle and proliferation analyses indicated that hypoSUMOylation potentiated Dex-induced cell cycle arrest and suppressed NALM6 cell proliferation, complementing the significant expression changes of cell cycle-related genes in our transcriptome data. Our work provides a valuable resource of GR chromatin partners and implies potential for targeting SUMOylation to increase sensitivity to GCs in ALL.
2025-01-20 | GSE233550 | GEO
Project description:The epigenetic process safeguards cell identity during cell division through the inheritance of appropriate gene expression profiles. We demonstrated previously that parental nucleosomes are inherited by the same chromatin domains during DNA replication only in the case of repressed chromatin. We now show that this specificity is conveyed by NPM1, a histone H3/H4 chaperone. Proteomic analyses of late S-phase chromatin revealed NPM1 in association with both H3K27me3, an integral component of facultative heterochromatin and MCM2, an integral component of the DNA replication machinery; moreover NPM1 interacts directly with PRC2 and with MCM2. Given that NPM1 is essential, the inheritance of repressed chromatin domains was examined anew using mESCs expressing an auxin-degradable version of endogenous NPM1. Upon NPM1 degradation, cells accumulated in S-phase of the cell-cycle and parental nucleosome inheritance from repressed chromatin domains was markedly compromised. Appropriate inheritance required the NPM1 acidic patches that function in chaperone activity, pointing to NPM1 being integral to the epigenetic process.
2022-04-27 | GSE183090 | GEO
Project description:CARM1 is an integral component of the NuRD chromatin remodeling complex (RNA-Seq)
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Project description:SUMOylation, a post-translational protein modification, is dramatically upregulated and critically involved in heat stress response conservatively among species. Previous studies in Arabidopsis indicated that numerous chromatin associated proteins are SUMOylation substrates and most of heat-enhancing SUMOylation reactions occur in nucleus. However, the global functional connection between gene expression regulation and SUMOylation on chromatin is completely unknown in plant cells. Here we show a genome-wide relationship of chromatin-associated SUMOylation and transcription switches under room temperature, heat stress, and recovering conditions in Arabidopsis. The SUMO-associated chromatin sites, characterized via whole-genome ChIP-seq assays, are generally correlated with active chromatin markers. In response to heat stress, we found chromatin-associated SUMO signals increased at promoter-transcriptional start site regions and decreased in the gene bodies. Further RNA-seq analysis supported the role of chromatin-associated SUMOylation in activation of transcription during rapid responses to high temperature. Changing of SUMO signals on chromatin is correlated with upregulation of heat-responsive genes and downregulation of growth-related genes. Disruption of the SUMO ligase gene SIZ1 abolishes SUMO signals on chromatin and attenuates the rapid transcriptional responses to heat stress. Interestingly, the SUMO signal peaks are enriched in DNA elements recognized by distinguished groups of transcription factors under different temperature conditions. Collectively, our data provide evidence that SUMOylation on chromatin regulates transcription switches during development and heat stress response, improving our understanding on the precise roles of SUMOylation in plant cells.
2020-08-04 | GSE140507 | GEO
Project description:Transcription factors represent one of the largest groups of proteins regulated by SUMO, and their modification has generally been correlated with transcriptional repression. However, as most of the studies focus on specific sumoylated transcriptional regulators, the distribution and global role of SUMO on chromatin in relation to transcription regulation remain largely unknown. To investigate this role, we determined the occupancy of SUMO machinery proteins on chromatin by ChIP coupled to sequencing in human primary cells. Examination of 3 histone modifications, Polymerase II, SUMO1, SUMO2, Ubc9 and PIASy in proliferative and Ras-induced senescent fibroblasts.
2013-07-24 | E-GEOD-42211 | biostudies-arrayexpress