Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA264081 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1614130.fastq.gz | Fastqsanger.gz | |||
| SRR1614131.fastq.gz | Fastqsanger.gz | |||
| SRR1614132.fastq.gz | Fastqsanger.gz | |||
| SRR1614133.fastq.gz | Fastqsanger.gz | |||
| SRR1614128.fastq.gz | Fastqsanger.gz |
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Project description: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.
2015-05-26 | GSE62428 | GEO
Project description:Truncating mutations of CHD8, encoding a chromodomain helicase, and of many other genes with diverse functions, are strong-effect risk factors for autism spectrum disorder (ASD), suggesting multiple mechanisms of pathogenesis. We explored the transcriptional networks that CHD8 regulates in neural progenitor cells (NPCs) by reducing its expression and then integrating transcriptome sequencing (RNA-seq) with genome-wide CHD8 binding (ChIP-seq). Suppressing CHD8 to levels comparable with loss of a single allele caused altered expression of 1,756 genes, 64.9% of which were up-regulated. CHD8 showed widespread binding to chromatin, with 7,324 replicated sites that marked 5,658 genes. Integration of these data suggests that a limited array of direct regulatory effects of CHD8 produced a much larger network of secondary expression changes. Genes indirectly down-regulated (i.e., without CHD8 binding sites) reflect pathways involved in brain development, including synapse formation, neuron differentiation, cell adhesion, and axon guidance, whereas CHD8-bound genes are strongly associated with chromatin modification and transcriptional regulation. Genes associated with ASD were strongly enriched among indirectly down-regulated loci (pM-BM- =M-BM- 1.01x10-9) and CHD8-bound genes (p = 4.34x10-3), which align with previously identified co-expression modules during fetal development. We also find an intriguing enrichment of cancer related gene-sets among CHD8-bound genes (p < 1.9x10-11). In vivo suppression of chd8 in zebrafish produced macrocephaly comparable to that of humans with inactivating mutations. These data indicate that heterozygous disruption of CHD8 precipitates a network of gene expression changes involved in neurodevelopmental pathways in which many ASD-associated genes may converge on shared mechanisms of pathogenesis. ChIP-seq for CHD8 using three different antibodies, and the related protein CHD7, in human iPSC-derived NPCs treated with shRNA targeting GFP (which were used as control cells for an shRNA knockdown RNA-seq experiment that was part of the overall study)
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Project description:Hypoxia-related Transcription factor ChIP-Seq data in T47D breast cancer cells
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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.
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