Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chip-seq analysis of CHD8 distribution in T47D cells

ABSTRACT: CHD8 is an ATPase of the SNF2 family involved in ATP-dependent nucleosome remodeling. Here we report data of the occupancy of CHD8 by ChIP-seq in human breast carcinoma T47D cells under different growing conditions. We show that under normal proliferation conditions CHD8 is mostly associated with promoters. Then, cells were subjected to 48 h or serum starvation followed by stimulation with the progesterone receptor (PR) agonist R5020 or with vehicle (ethanol), for 5 and 45 minutes. R5020 induced the fast association of CHD8 with a number of intergenic or intronic regions. We found that these regions were enriched in PR binding sites. Furthermore, they were enriched in H3K4me1 and P300, typical markers of enhancers. Therefore, our data indicate that in the presence of the PR agonist CHD8 is recruited to a number of PR enhancers. In additional experiments we demonstrated that CHD8 is required for activation of PR enhancers and for transcriptional regulation of progesterone-dependent genes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE62428 | GEO | 2015/05/26

SECONDARY ACCESSION(S): PRJNA264081

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

CHD8 controls progestin-dependent gene expression in T47D cells

Project description:CHD8 is an ATPase of the SNF2 family involved in ATP-dependent nucleosome remodeling. Our data indicate that in the presence of progestin (R5020), a progesterone receptor (PR) agonist, CHD8 is recruited to a number of PR enhancers. To correlate CHD8 binding sites with CHD8-regulated gene expression we performed a transcriptomic analysis of T47D-MTVL cells transfected with a control siRNA or a siRNA specifically targeting CHD8 and stimulated during 6h with progestin or vehicle. CHD8-dependent genes presented lower induction of up-regulated genes and lower repression of down-regulated genes, indicating that CHD8 is required for progesterone-dependent regulation of a subset of genes.

2015-06-01 | GSE62257 | GEO

ER/PR RIME Experiments in MCF7 and T47D cell lines

Project description:Immuno-precipitation followed by MS was performed using the RIME protocol in this study. Estrogen Receptor (ER) and Progestorone Receptor (PR) were targetted using antibodies. The experiments were performed in a quantitative manner using SILAC labelling. Cells grown in complete serum (estrogenic) conditions were compared against an cells in similar complete media, however supplemented with Progesterone (PG) or R5020 for 4 hours. Experiments were performed in MCF7 and T47D cell lines

2015-05-26 | PXD002104 | Pride

Genes differentially expressed upon CHD8 knockdown

2009-05-01 | GSE11422 | GEO

shRNAi profiling of huuman CHD8 depleted cells

Project description:CHD8 is a putative chromatin remodeling ATPase of the SNF2 family. We found that depletion of CHD8 impairs cell proliferation. In order to identify CHD8 target genes, we performed a transcriptomic analysis of CHD8-depleted cells. CHD8 was knockdown by doxycyclin-dependent expression of a shRNA that target the CHD8 mRNA. Experiment Overall Design: C33KD2 is a stable cell line where expression of a shRNA, that targets the CHD8 mRNA, is dependent on doxycycline. Addition of doxyclycin provokes a significant reduction in the level of CHD8 protein. Total RNA samples coming from C33KD2 cells cultured for 48 hours either with or without 2 µg/ml doxycycline were used to generate complementary RNA labelled with Cy5 with the Agilent Low RNA Input Fluorescent Linear Amplification Kit (Agilent Technologies). The reference sample was Stratagene human universal reference and was amplified at the same time as the sample RNA using the same method. Reference samples were labeled using Cy3.

2009-05-14 | E-GEOD-11422 | biostudies-arrayexpress

Genomic agonism and phenotypic antagonism between estrogen and progesterone receptors in breast cancer. [ChIP-seq]

Project description:Transcriptomic changes and estrogen and progesterone receptor binding in multiple ER+/PR+ models (eight ER+/PR+ patient tumors, various T47Ds, ZR75) and multiple ER+/PR-negative models (four ER+/PR- patient tuumors, PR-deficient T47D and MCF7 cells) treated with various hormone combinations. Results: In isolation, estrogen and progestin act as genomic agonists by regulating the expression of common target genes in similar directions, but at different levels. Similarly, in isolation, progestin is also a weak phenotypic agonist of estrogen action. However, in the presence of both hormones, progestin behaves as a phenotypic estrogen antagonist. PR remodels nucleosomes to noncompetitively redirect ER genomic binding to distal enhancers enriched for BRCA1 binding motifs and sites that link PR and ER/PR complexes. Importantly, when both hormones are present, progestin modulates estrogen action such that responsive transcriptomes, cellular processes and ER/PR recruitment to genomic sites correlate with those observed with PR alone, but not ER alone. Conclusions: Genomic Agonism and Phenotypic Antagonism between Estrogen and Progesterone Receptors in Breast Cancer. Individual and concerted actions of ER and PR highlight the prognostic and therapeutic value of PR in ER+/PR+ breast cancers. ER+/PR+ and ER+/PR-deficient model systems were deprived of steroids by culturing them in phenol red free RPMI 1640 media that is supplemented with 10% charcoal-stripped fetal bovine serum and 1% penicillin/streptomycin. Subsequently, these steroid-deprived models were treated with either vehicle, 10 nM estradiol, 10 nM progestin R5020 or 10 nM of both the hormones and genomics (ChIP-seq and RNA-seq) was performed. ChIP-seq was done after 45 minutes of hormone treatments. For cell models, RNA-seq was done after 12 hours of hormone treatments. Tumor explants were treated with either 24 or 48 hours.

2016-06-01 | E-GEOD-80367 | biostudies-arrayexpress

Genomic agonism and phenotypic antagonism between estrogen and progesterone receptors in breast cancer. [tumor samples RNA-seq]

2016-06-01 | E-GEOD-80365 | biostudies-arrayexpress

Genomic agonism and phenotypic antagonism between estrogen and progesterone receptors in breast cancer. [cell models RNA-seq]

2016-06-01 | E-GEOD-80366 | biostudies-arrayexpress

Nucleosome driven transcription factor binding and gene regulation [ChIP-Seq]

Project description:Elucidating the global function of a transcription factor implies the identification of its target genes and genomic binding sites. The role of chromatin in this context is unclear, but the dominant view is that factors bind preferentially to nucleosome-depleted regions, identified as DNaseI-hypersensitive sites (DHS). Here we show by chromatin-IP, MNase and DNaseI assays followed by deep sequencing that the progesterone receptor (PR) requires nucleosomes for optimal binding and function. In breast cancer cells treated with progestins we identified 25,000 PR binding sites (PRbs), the majority encompassing several copies of the hexanucleotide TGTYCY, highly abundant in the genome. We found that functional PRbs accumulate around progesterone-induced genes mainly in enhancers, are enriched in DHS but exhibit high nucleosome occupancy. Progestin stimulation results in remodeling of these nucleosomes with displacement of histones H1 and H2A/H2B dimers. Our results strongly suggest that nucleosomes are crucial for PR binding and hormonal gene regulation. T47D-MTVL human breast cancer cells were incubated with the progestin R5020 for different times between 0 to 360 minutes at 37ÂºC. ChIP-seq experiments were performed using antibodies against progesterone receptor and a single Sample each with anti-H3K4me3 and anti-H3K4me1. Mononucleosomal DNA was prepared from cells untreated or stimulated 60 min with R5020 and subjected to deep sequencing using the Solexa Genome Analyzer.

2012-12-01 | E-GEOD-41466 | biostudies-arrayexpress

The chromatin modifier CHD8 targets autism risk genes during human neurodevelopmentM-BM-

Project description:Whole-exome sequencing studies have implicated chromatin modifiers and transcriptional regulators in autism spectrum disorder (ASD) through the identification of de novo loss of function mutations in affected individuals. Many of these genes are co-expressed in mid-fetal human cortex, suggesting ASD risk genes converge in regulatory networks that are perturbed in ASD during neurodevelopment. To elucidate such networks we mapped promoters and enhancers bound by the chromodomain helicase CHD8, which is strongly enriched in ASD-associated de novo loss of function mutations, using ChIP-seq in mid-fetal human brain, human neural stem cells (hNSCs), and embryonic mouse cortex. We find that CHD8 targets are strongly enriched for ASD risk genes that converge in ASD-associated co-expression networks in human midfetal cortex. CHD8 knockdown in hNSCs results in significant dysregulation of ASD risk genes targeted by CHD8, as well as additional genes important for neurodevelopment, including members of the Wnt/M-NM-2-catenin signaling pathway. Integration of CHD8 binding data with genetic and gene co-expression data in ASD risk models provides support for additional ASD risk genes. Together, our results suggest that loss of CHD8 function contributes to ASD through regulatory perturbation of other ASD risk genes during human cortical development. Two biological replicates for each ChIP with appropriate Input control Four biological replicates for each condition in knockdown experiments (Ctrl construct, Chd8 target C, and Chd8 target G)

2015-01-21 | E-GEOD-57369 | biostudies-arrayexpress

ChIP-seq of ER, PR, p300 in two ER+ breast cancer cell lines treated with estrogen and with and without progestins

Project description:Exploring effect of progesterone/progestin treatment on ER and PR binding. Two cell lines, three conditions (Full Media with E2, E2+ Progesterone, Full Media + R5020 Progestin), three factors (ER, PR, p300), all with three replicates, each with a matched Input control.

2015-05-22 | E-GEOD-68355 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data