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Influence of SUMOylation on chromatin structure in hIPSCs (ChiPS4) assessed by time-resolved ATAC-seq in response to ML792 treatment

ABSTRACT: Influence of SUMOylation on chromatin structure in hIPSCs (ChiPS4) assessed by time-resolved ATAC-seq in response to ML792 treatment

PROVIDER: PRJEB42229 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR5022190_1.fastq.gz	Fastqsanger.gz
	ERR5022190_2.fastq.gz	Fastqsanger.gz
	ERR5022200_1.fastq.gz	Fastqsanger.gz
	ERR5022200_2.fastq.gz	Fastqsanger.gz
	ERR5022191_1.fastq.gz	Fastqsanger.gz

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Influence of SUMOylation on chromatin structure in hIPSCs (ChiPS4) assessed by time-resolved ATAC-seq in response to ML792 treatment

Project description:SUMOylation is thought to regulate chromatin structure and accessibility thus affecting gene expression. In order to assess these potential roles of SUMOylation in human pluripotent stem cells, ChiPS4 cells were treated with ML792 (selective SUMO E1 inhibitor) or DMSO (vehicle control) for the following times: 4, 8, 24 and 48h or left untreated for 48h. At each time point samples were collected for western blotting (control for the efficacy of treatment), RNA-seq (total RNA extracted using RNeasy Mini Kit) and ATAC-seq (using Omni-ATAC protocol, 3 replicates for each time point). Samples were further used for library preparation and sequenced using the Illumina NovaSeq 6000 S4.

2022-12-01 | E-MTAB-9961 | biostudies-arrayexpress

Influence of SUMOylation on transcriptional signature of hIPSCs (ChiPS4) assessed by time-resolved RNA-seq in response to ML792 treatment

Project description:Influence of SUMOylation on transcriptional signature of hIPSCs (ChiPS4) assessed by time-resolved RNA-seq in response to ML792 treatment

| PRJEB42228 | ENA

Influence of SUMOylation on transcriptional signature of hIPSCs (ChiPS4) assessed by time-resolved RNA-seq in response to ML792 treatment

Project description:SUMOylation is thought to regulate chromatin structure and accessibility thus affecting gene expression. In order to assess these potential roles of SUMOylation in human pluripotent stem cells, ChiPS4 cells were treated with ML792 (selective SUMO E1 inhibitor) or DMSO (vehicle control) for the following times: 4, 8, 24 and 48h. At each time point samples were collected for western blotting (control for the efficacy of treatment), RNA-seq (total RNA extracted using RNeasy Mini Kit, samples in 4 replicates per time point) and ATAC-seq (using Omni-ATAC protocol). Samples were further used for library preparation and sequenced using the Illumina NovaSeq 6000 S4.

2022-12-01 | E-MTAB-9962 | biostudies-arrayexpress

Landscape of protein SUMOylation on chromatin in hIPSCs (ChiPS4) by SUMO1 CHIP-seq

Project description:Landscape of protein SUMOylation on chromatin in hIPSCs (ChiPS4) by SUMO1 CHIP-seq

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Landscape of protein SUMOylation on chromatin in hIPSCs (ChiPS4) by SUMO1 CHIP-seq

Project description:SUMO1 CHIP-seq experiment was performed in untreated hiPSC line - ChiPS4, to determine the exact locations of chromatin bound SUMO1 in these cells, thus providing information about the landscape of SUMOylation of protein targets on chromatin in human pluripotent cells and as such allowing for investigation of the role of SUMO1 in regulation of chromatin state.

2022-12-01 | E-MTAB-9960 | biostudies-arrayexpress

E-MTAB-9962

Project description:Influence of SUMOylation on transcriptional signature of hIPSCs (ChiPS4) assessed by time-resolved RNA-seq in response to ML792 treatment

2025-01-23 | E-MTAB-9962 | ExpressionAtlas

Genome-wide analysis of androgen receptor (AR) SUMOylation effects on gene expression (HEK293).

Project description:Androgen receptor (AR) plays an important regulatory role during prostate cancer development. ARM-bM-^@M-^Ys transcriptional activity is regulated by androgenic ligands, but also by post-translational modifications. To study the role of the AR SUMOylation in genuine chromatin environment, we compared androgen-regulated gene expression and AR chromatin occupancy in PC-3 prostate cancer and HEK293 cell lines stably expressing wild-type (wt) or SUMOylation site-mutated AR (AR-K386R,K520R). Our genome-wide gene expression analyses reveal that the SUMOylation modulates the AR function in a target gene and pathway selective manner. The transcripts that are differentially regulated by androgen and SUMOylation are linked to cellular movement, cell death, cellular proliferation, cellular development and cell cycle. In line with these data, SUMOylation mutant AR cells proliferate faster and are more sensitive to apoptosis. Moreover, ChIP-seq analyses show that the SUMOylation modulates the chromatin occupancy of AR on many loci in a fashion that parallels with their differential androgen-regulated expression. De novo motif analyses show that other transcription factor-binding motifs are differentially enriched at the wtAR- and the AR-K386R,K520R-preferred genomic binding positions. Taken together, our data indicate that SUMOylation does not simply repress the AR activity, but it regulates ARM-bM-^@M-^Ys interaction with the chromatin and the receptorM-bM-^@M-^Ys target gene selection. Isogenic HEK293 cells stably expressing wild-type AR (wtAR) or SUMOylation-defective AR (AR-K2R) were treated 24 h with 10 nM R1881 or vehicle (EtOH). All conditions were performed in triplicate. The effect on gene expression was assessed by microarray.

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2014-01-25 | E-MTAB-2138 | biostudies-arrayexpress

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Project description:Androgen receptor (AR) plays an important regulatory role during prostate cancer development. ARM-bM-^@M-^Ys transcriptional activity is regulated by androgenic ligands, but also by post-translational modifications. To study the role of the AR SUMOylation in genuine chromatin environment, we compared androgen-regulated gene expression and AR chromatin occupancy in PC-3 prostate cancer and HEK293 cell lines stably expressing wild-type (wt) or SUMOylation site-mutated AR (AR-K386R,K520R). Our genome-wide gene expression analyses reveal that the SUMOylation modulates the AR function in a target gene and pathway selective manner. The transcripts that are differentially regulated by androgen and SUMOylation are linked to cellular movement, cell death, cellular proliferation, cellular development and cell cycle. In line with these data, SUMOylation mutant AR cells proliferate faster and are more sensitive to apoptosis. Moreover, ChIP-seq analyses show that the SUMOylation modulates the chromatin occupancy of AR on many loci in a fashion that parallels with their differential androgen-regulated expression. De novo motif analyses show that other transcription factor-binding motifs are differentially enriched at the wtAR- and the AR-K386R,K520R-preferred genomic binding positions. Taken together, our data indicate that SUMOylation does not simply repress the AR activity, but it regulates ARM-bM-^@M-^Ys interaction with the chromatin and the receptorM-bM-^@M-^Ys target gene selection. PC-3 cells stably expressing wild-type AR (wtAR) or SUMOylation-defective AR (AR-K2R) were treated 16 h with 10 nM R1881 or vehicle (EtOH). All conditions were performed in triplicate. The effect on gene expression was assessed by microarray.

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