CHD7 Regulates Definitive Endodermal and Mesodermal Development from Human Embryonic Stem Cells [RNAseq]
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ABSTRACT:
PROVIDER: PRJNA1152887 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30413003_1.fastq.gz | Fastqsanger.gz | |||
| SRR30413003_2.fastq.gz | Fastqsanger.gz | |||
| SRR30413004_1.fastq.gz | Fastqsanger.gz | |||
| SRR30413004_2.fastq.gz | Fastqsanger.gz | |||
| SRR30413005_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:CHD7 Regulates Definitive Endodermal and Mesodermal Development from Human Embryonic Stem Cells [ATACseq]
| PRJNA1152886 | 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: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:RNAseq of iPSC derived pulmonary organoids by co-culturing endodermal and mesodermal progenitors
| PRJEB56634 | ENA
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:The directed differentiation of induced pluripotent stem (iPS) and embryonic stem (ES) cells into definitive endoderm (DE) would allow the derivation of otherwise inaccessible progenitors for endodermal tissues. However, a global comparison of the relative equivalency of DE derived from iPS and ES populations has not been performed. Recent reports of molecular differences between iPS and ES cells have raised uncertainty as to whether iPS cells could generate autologous endodermal lineages in vitro. Here, we have shown that both mouse iPS and parental ES cells exhibited highly similar in vitro capacity to undergo directed differentiation into DE progenitors. With few exceptions, both cell types displayed similar surges in gene expression of specific master transcriptional regulators and global transcriptomes that define the developmental milestones of DE differentiation. Microarray analysis showed considerable overlap between the genetic programs of DE derived from ES/iPS cells in vitro and authentic DE from mouse embryos in vivo. Intriguingly, iPS cells exhibited aberrant silencing of imprinted genes known to participate in endoderm differentiation, yet retained a robust ability to differentiate into DE. Our results show that, despite some molecular differences, iPS cells can be efficiently differentiated into DE precursors, reinforcing their potential for development of cell-based therapies for diseased endodermal-derived tissues. Comparison of mouse ES cells, mouse iPS cells, and E8.25 Mouse embryos; in the undifferentiated state and definitive endoderm differentiated state. ckit+/Sox2dim =definitive endoderm (day 5 of differentiation in vitro); Sox2bright =undifferentiated ES or iPS cells (day 0 of differentiation); ENDM1+/Epcam+/SSlo=foregut endoderm sorted from mouse E8.25 embryos; Epcam+/ENDM1 negative =sorted comparison population from mouse E8.25 embryos.
2011-03-31 | E-GEOD-27087 | biostudies-arrayexpress
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:Post-translational modifications of proteins are crucial to the regulation of their activity and function. As a newly discovered acylation modification, crotonylation of non-histone proteins remains largely unexplored, particularly in human embryonic stem cells (hESCs). Here we report the investigation of induced crotonylation in hESCs, which resulted in hESCs of different pluripotency states differentiating into the endodermal lineage. We showed that increased protein crotonylation in hESCs was accompanied by transcriptomic shifts and decreased glycolysis. Through large-scale profiling of non-histone protein crotonylation, we identified metabolic enzymes as major targets of inducible crotonylation in hESCs. We further discovered GAPDH as a key glycolytic enzyme regulated by crotonylation during endodermal differentiation from hESCs, where crotonylation of GAPDH decreased its enzymatic activity thereby leading to reduced glycolysis. Our study demonstrates that crotonylation of glycolytic enzymes may be crucial to metabolic switching and cell fate determination in hESCs.
2022-10-27 | PXD027007 | Pride