CHD7 Regulates Definitive Endodermal and Mesodermal Development from Human Embryonic Stem Cells [ATACseq]
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ABSTRACT:
PROVIDER: PRJNA1152886 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30412064_1.fastq.gz | Fastqsanger.gz | |||
| SRR30412064_2.fastq.gz | Fastqsanger.gz | |||
| SRR30412065_1.fastq.gz | Fastqsanger.gz | |||
| SRR30412065_2.fastq.gz | Fastqsanger.gz | |||
| SRR30412066_1.fastq.gz | Fastqsanger.gz |
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Project description:CHD7 encodes an ATP-dependent chromodomain helicase DNA binding protein; mutations in this gene lead to multiple developmental disorders, including CHARGE (Coloboma, Heart defects, Atresia of the choanae, Retardation of growth and development, Genital hypoplasia, and Ear anomalies) syndrome. How the mutations cause multiple defects remains largely unclear. Embryonic definitive endoderm (DE) generates the epithelial compartment of vital organs such as the thymus, liver, pancreas, and intestine. In this study, we used clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 technique to delete the CHD7 gene in human embryonic stem cells (hESCs) to generate CHD7 homozygous mutant (CHD7-/-), heterozygous mutant (CHD7+/-), and control wild-type (CHD7+/+) cells. We then investigated the ability of the hESCs to develop into DE and the other two germ layers, mesoderm and ectoderm. We found that deletion of CHD7 led to reduced capacity to develop into DE and mesoderm in a dose-dependent manner. To determine the underlying mechanisms, we compared global gene expression and chromatin accessibility among the hESC-DE cells by RNA sequencing (RNA-seq) and the assay for transposase-accessible chromatin with sequencing (ATAC-seq). We found that loss of CHD7 led to significant changes in the expression and chromatin accessibility of genes associated with several pathways. We identified 40 genes that were highly down-regulated in both the expression and chromatin accessibility in CHD7 deleted hESC-DE cells. Our results provide new insights into the mechanisms by which CHD7 mutations cause multiple congenital anomalies.
2025-05-27 | GSE275739 | GEO
Project description:CHD7 Regulates Definitive Endodermal and Mesodermal Development from Human Embryonic Stem Cells [RNAseq]
| PRJNA1152887 | ENA
Project description:CHD7 encodes an ATP-dependent chromodomain helicase DNA binding protein; mutations in this gene lead to multiple developmental disorders, including CHARGE (Coloboma, Heart defects, Atresia of the choanae, Retardation of growth and development, Genital hypoplasia, and Ear anomalies) syndrome. How the mutations cause multiple defects remains largely unclear. Embryonic definitive endoderm (DE) generates the epithelial compartment of vital organs such as the thymus, liver, pancreas, and intestine. In this study, we used clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 technique to delete the CHD7 gene in human embryonic stem cells (hESCs) to generate CHD7 homozygous mutant (CHD7-/-), heterozygous mutant (CHD7+/-), and control wild-type (CHD7+/+) cells. We then investigated the ability of the hESCs to develop into DE and the other two germ layers, mesoderm and ectoderm. We found that deletion of CHD7 led to reduced capacity to develop into DE and mesoderm in a dose-dependent manner. To determine the underlying mechanisms, we compared global gene expression and chromatin accessibility among the hESC-DE cells by RNA sequencing (RNA-seq) and the assay for transposase-accessible chromatin with sequencing (ATAC-seq). We found that loss of CHD7 led to significant changes in the expression and chromatin accessibility of genes associated with several pathways. We identified 40 genes that were highly down-regulated in both the expression and chromatin accessibility in CHD7 deleted hESC-DE cells. Our results provide new insights into the mechanisms by which CHD7 mutations cause multiple congenital anomalies.
2025-05-27 | GSE275741 | GEO
Project description:Endodermal progenitor cells (EP cells) are derived from human embryonic stem cell(ESC)-derived definitive endoderm (DE) cells. EP cells are cultured in high BMP media and DE cells are in high Activin media. Both cells can be further differentiated to liver, pancreas, etc. We used microarray to detail the global gene expression profile of DE cells and EP cells to delineate the difference of DE cells and EP cells.
2012-02-01 | GSE35461 | GEO
Project description:Endodermal progenitor cells (EP cells) are derived from human embryonic stem cell(ESC)-derived definitive endoderm (DE) cells. EP cells are cultured in high BMP media and DE cells are in high Activin media. Both cells can be further differentiated to liver, pancreas, etc. We used microarray to detail the global gene expression profile of DE cells and EP cells to delineate the difference of DE cells and EP cells. ESCs were sorted by SSEA3 and SSEA4. DE cells and EP cells were sorted by CXCR4 and CD117. Sorted cells were lysed in RLT buffer. RNA was extracted and hybridized to Affimetrix microarrays. Each group had 3 biological replicates.
2012-02-01 | E-GEOD-35461 | biostudies-arrayexpress
Project description:This study will analyse the global RNA expression patterns in human iPSC and endodermal differentiated cells.The goal of this project is to investigate genes regulating definitive endodermal differentiation of human iPSC using genetic screening. The differentiation of human iPSC into definitive endoderm is going to be examined by global RNA expression patterns. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/
2015-06-09 | E-ERAD-363 | biostudies-arrayexpress
Project description:RNAseq of iPSC derived pulmonary organoids by co-culturing endodermal and mesodermal progenitors
| PRJEB56634 | ENA
Project description:CHD7 is a member of the chromodomain helicase DNA binding domain family of ATP-dependent chromatin remodeling enzymes. De novo mutation of the CHD7 gene is a major cause of CHARGE syndrome, a genetic disease characterized by a complex constellation of birth defects. To gain insight to the function of CHD7, we mapped the distribution of the CHD7 protein on chromatin using the approach of chromatin immunoprecipitation on tiled microarrays (ChIP-chip). These studies were performed in human colorectal carcinoma cells, human neuroblastoma cells, and mouse embryonic stem (ES) cells before and after differentiation into neural precursor cells. The results indicate that CHD7 localizes to discrete locations along chromatin that are specific to each cell type, and that the cell-specific binding of CHD7 correlates with a subset of histone H3 methylated at lysine 4 (H3K4me). The CHD7 sites change concomitantly with H3K4me patterns during ES cell differentiation, suggesting that H3K4me is part of the epigenetic signature that defines lineage-specific association of CHD7 with specific sites on chromatin. Furthermore, the CHD7 sites are predominantly located distal to transcription start sites, most often contained within DNase hypersensitive sites, frequently conserved, and near genes expressed at relatively high levels. These features are similar to those of gene enhancer elements, raising the possibility that CHD7 functions in enhancer mediated transcription, and that the congenital anomalies in CHARGE syndrome are due to alterations in transcription of tissue-specific genes normally regulated by CHD7 during development. ChIP-chip experiments were performed for CHD7 and H3K4 mono-,di-, and trimethylation modifications in 4 cells types: human DLD1 and SH-SY5Y; mouse ES and differentiated neural precursor cells derived from mouse ES cells. Microarrays used in these experiments tiled all or subset of ENCODE regions (in mouse, analogous ENCODE regions were assayed). At least two biological replicates were performed for each CHD7 ChIP experiment; H3K4 ChIP's were performed once in each cell type.
2009-01-22 | E-GEOD-14460 | biostudies-arrayexpress
Project description:Gene expression changes were measured between mouse ES cells of three genotypes: WT Chd7, Heterzygous Chd7 Null, Homozygous Chd7 Null. The hypothesis being tested was that CHD7, a chromatin remodeling protein, functions as a transcriptional regulator. This experiment was performed to detect gene targets of CHD7-mediated regulation. We report the genome-wide binding profile of CHD7, the protein implicated in CHARGE syndrome, in mouse ES cells using ChIP-Seq technology. Combining these data with other genomic datasets, we discover CHD7 to colocalize with other transcription factors including Oct4, Nanog, Sox2, and p300 at gene enhancer elements to regulate ES cell specific gene expression. Chd7 wildtype, heterozygous, and homozygous ES cells derived from preimplantation embryos were grown on feeder cells and total RNA was isolated using Trizol. The ratio of ES to feeder cells was estimated at 5:1. ChIP sequencing of CHD7 and p300 in mouse ES cells
2010-06-15 | E-GEOD-22341 | biostudies-arrayexpress
Project description:The ability of human induced pluripotent stem cells (hiPSCs) to differentiate in vitro to each of the three germ layer lineages has made them an important developmental model and tool for tissue engineering. Here we explore the impact of inducing DNA damage at different points during differentiation. We show that, during a critical window in this program, DNA damage diverts cells from an endodermal to mesodermal fate without significant upregulation of an apoptotic program. This change in transcriptional program is driven by p53: cells lacking p53 continue to differentiate towards endoderm with high efficiency despite significant genomic damage and G2/M cell cycle arrest. Thus, DNA damage-induced upregulation of p53 decreases the efficiency of hiPSC differentiation to definitive endoderm by diverting cells towards a mesodermal fate.
2020-07-27 | GSE146225 | GEO