Genome-wide chromatin accessibility in pluripotent and surface ectoderm cells with and without p63
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ABSTRACT:
PROVIDER: PRJNA491198 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7839290_1.fastq.gz | Fastqsanger.gz | |||
| SRR7839290_2.fastq.gz | Fastqsanger.gz | |||
| SRR7839291_1.fastq.gz | Fastqsanger.gz | |||
| SRR7839291_2.fastq.gz | Fastqsanger.gz | |||
| SRR7839292_1.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: Evaluate changes in chromatin accessibility between human embryonic stem cells and surface ectoderm cells with and without the transcription factor p63. Method: Chromatin accessibility profiles for human embryonic stem cells and surface ectoderm with and without p63 were generated by deep sequencing, in duplicate, with the Illumina NextSeq sequencer. Quality reads were assessed by fastq. Reads were aligned using Bowtie2, PCR duplicates and mitochondrial DNA were discarded, and peak calling was completed using MACS2. Non-reproducible peaks were filtered out by IDR with an FDR of 5%. Results: p63 fails to modify chromatin accessibility when ectopically expressed in human embryonic stem cells; differentiation of human embryonic stem cells to surface ectoderm results in the closure of some regions open in pluripotent cells and the opening of new regions; and loss of p63 in the surface ectoderm results in increased accessibility of 1/3 of the regions opened during surface ectoderm differentiation. Conclusion: p63's ability to modify chromatin accessibility is dependent upon the underlying epigenetic landscape, and when it can modify the landscape, it does so by closing regions that become open during ectoderm differentiation.
2018-11-06 | GSE119996 | GEO
Project description:Purpose: Assess changes in the three-dimensional (3D) chromatin architecture during surface ectoderm commitment and evaluate changes in 3D chromatin architecture in human embryonic stem cells and surface ectoderm cells with and without p63. Methods: Cohesin HiChIP profiles for human embryonic stem cells and surface ectoderm cells with and without p63 were generated in triplicate with deep sequencing on the Illumina HiSeq 4000 sequencer. Using HiC-Pro, paired end reads were aligned to hg19, duplicate reads were removed, and then were assigned to MboI restriction fragments, filtered for valid interactions, and used to generate binned interaction matrices of 10 kb resolution. Contacts were called using FitHiC and filtered for counts >= 10 and FDR < 0.001. Results: The greatest change in 3D chromatin architecture was observed between human embryonic stem cells and surface ectoderm cells, while moderate changes were observed in human embryonic stem cells with and without p63, and limited changes were observed in surface ectoderm cells with and without p63. Conclusion: Both p63 and the surface ectoderm morphogens direct changes in chromatin folding to establish the 3D chromatin landscape in the surface ectoderm.
2018-11-06 | GSE120294 | GEO
Project description:Purpose: Evaluate p63 regulation of gene expression in human embryonic stem cells and the surface ectoderm Methods: RNA profiles for human embyronic stem cells and surface ectoderm cells with and without p63 using deep sequencing, in duplicate, on Illumina NextSeq 500 sequencer. Quality of reads were checked by fastqc. Reads were aligned to hg19 genome using tophat and FPKM values were generated using Homer. Results: p63 is largely unable to regulate gene expression in pluripotent cells, but acts primarily as a repressor in the surface ectoderm. Conclusion: p63 regulation of gene expression is dependent on the changes the cell undergoes during surface ectoderm commitment
2018-11-06 | GSE121994 | GEO
Project description:Purpose: Validate HiChIP-identified long-range chromatin interactions at the TFAP2C locus, in a viewpoint-specific manner. Methods: UMI-4C libraries targeting 3 individual viewpoints at the TFAP2C locus were generated in duplicate, in surface ectoderm cells with and without p63. Replicates were sequenced on Illumina NextSeq sequencer, and reads were aligned and filtered for valid long-range interactions using HiCPro. Results: Dynamic long-range interactions at the TFAP2C locus were detected with and without p63 in surface ectoderm cells. Conclusion: Long-range interactions detected via HiChIP were confirmed in the surface ectoderm by this technique, validating the HiChIP method through an orthogonal approach.
2018-11-06 | GSE114846 | GEO
Project description:RNA-seq profiles of pluripotent and surface ectoderm cells with and without p63
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Project description:Cohesin HiChIP datasets of pluripotent and surface ectoderm cells with and without p63
| PRJNA492416 | ENA
Project description:UMI-4C in wild-type and p63-null surface ectoderm cells
| PRJNA472808 | ENA
Project description:Purpose: Assess changes in p63 binding in human embryonic stem cells and surface ectoderm; evaluate differences in the following histone marks: H3K27me3, H3K27ac, H3K4me1, and H3K4me3 in the surface ectoderm with and without p63; and examine changes in H3K27me3 between human embyronic stem cells and surface ectoderm with and without p63. Methods: p63 ChIP-seq libraries were generated in p63 gain-of-function human embryonic stem cells and wild-type surface ectoderm. H3K27me3 ChIP-seq libraries were generated in wild-type and p63 gain-of-function human embryonic stem cells as well as wild-type and p63 knockout surface ectoderm. H3K27ac, H3K4me1, and H3K4me3 ChIP-seq libraries were generated in wild-type and p63 knockout surface ectoderm. All ChIP-seq experiments were performed in duplicate and sequenced on Illumina NextSeq 500 sequencer. To ensure quality reads, fastq files were analyzed using FASTQC. Bowtie was used for read mapping and the parameters were as follows: -p 24 -S -a -m 1 --best --strata. For peak calling using MACS2, default settings were specified with a p-value of 0.05. To ensure quality peaks, IDR was run on all files, specifying FDR of 1% or 5% (or 10% for some broadPeak histone marks). Results: Limited changes in p63 binding in human embryonic stem cells and surface ectoderm; global loss of H3K37me3 without p63 in the surface ectoderm; limited differences in H3K27ac, H3K4me1, and H3K4me3 +/- p63 in the surface ectoderm; and increase in H3K27me3 with ectopic expression of p63 in human embryonic stem cells. Conclusion: p63 is able to bind it's surface ectoderm target sites regardless of the epigenetic landscape; p63 promotes H3K27me3 accumulation; and p63 does not regulate histone marks H3K27ac, H3K4me1, or H3K4me3
2018-11-06 | GSE122128 | GEO
Project description:The transcription factor p63 is a master regulator of ectoderm development essential for epidermal specification. Although previous studies have highlighted the role of p63 triggering the epidermal transcriptomic program, its precise mechanism of target gene regulation in the complex context of a developing embryo remains poorly understood. Here, we used zebrafish embryos to analyze in vivo how p63 regulates the expression of its target genes during development. We generated tp63-knock-out mutants that recapitulate human phenotypes and show down-regulated epidermal gene expression. Following p63-binding dynamics during development, we found two distinct functions clearly separated in space and time. During early development, p63 binds enhancers associated to neural genes, where it limits Sox3 binding and reduces the expression of these neural genes. Indeed, we show that p63 and Sox3 are co-expressed in the neural plate border. Later in development, p63 binds enhancers associated to epidermal genes and promotes their expression, acting as a pioneer factor, as it binds to non-accessible chromatin and is required for its opening. Therefore, our results suggest that p63 is an important regulator of cell fate decisions during ectoderm specification, promoting the epidermal fate and inhibiting the neural program.
2019-06-06 | GSE123056 | GEO
Project description:The transcription factor p63 is a master regulator of ectoderm development essential for epidermal specification. Although previous studies have highlighted the role of p63 triggering the epidermal transcriptomic program, its precise mechanism of target gene regulation in the complex context of a developing embryo remains poorly understood. Here, we used zebrafish embryos to analyze in vivo how p63 regulates the expression of its target genes during development. We generated tp63-knock-out mutants that recapitulate human phenotypes and show down-regulated epidermal gene expression. Following p63-binding dynamics during development, we found two distinct functions clearly separated in space and time. During early development, p63 binds enhancers associated to neural genes, where it limits Sox3 binding and reduces the expression of these neural genes. Indeed, we show that p63 and Sox3 are co-expressed in the neural plate border. Later in development, p63 binds enhancers associated to epidermal genes and promotes their expression, acting as a pioneer factor, as it binds to non-accessible chromatin and is required for its opening. Therefore, our results suggest that p63 is an important regulator of cell fate decisions during ectoderm specification, promoting the epidermal fate and inhibiting the neural program.
2019-06-06 | GSE123057 | GEO