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CHD8 safeguards early neuroectoderm differentiation in human ESCs and protects from apoptosis during neurogenesis

ABSTRACT: CHD8 safeguards early neuroectoderm differentiation in human ESCs and protects from apoptosis during neurogenesis

PROVIDER: PRJNA721224 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14209407_1.fastq.gz	Fastqsanger.gz
	SRR14209407_2.fastq.gz	Fastqsanger.gz
	SRR14209408_1.fastq.gz	Fastqsanger.gz
	SRR14209408_2.fastq.gz	Fastqsanger.gz
	SRR14209409_1.fastq.gz	Fastqsanger.gz

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CHD8 safeguards early neuroectoderm differentiation in human ESCs and protects from apoptosis during neurogenesis

Project description:To understand the function of CHD8 in human ESC and neural differentiation, we generated the CHD8 knockout human ESCs and characterize the effect of loss-of-function of CHD8 on pluripotency maintenance and neuroectoderm determination by utilizing an efficient neuroectoderm differentiation protocol. Samples from hESC, CHD8KO_hESC and their derived-neural progenitor cells (hNPC) were collected for high-throughput sequencing with at least two replicates for each sample. Differentially expressed genes analysis showed loss of CHD8 affect the genes in ESC and NPC.

2021-10-19 | GSE171869 | GEO

CHD8 safeguards early neuroectoderm differentiation in human ESCs and protects from apoptosis during neurogenesis.

Project description:The chromatin remodeler CHD8, which belongs to the ATP-dependent chromatin remodelers CHD family, is one of the most high-risk mutated genes in autism spectrum disorders. However, the role of CHD8 in neural differentiation and the mechanism of CHD8 in autism remains unclear, despite there are a few studies based on the CHD8 haploinsufficient models. Here, we generate the CHD8 knockout human ESCs by CRISPR/Cas9 technology and characterize the effect of loss-of-function of CHD8 on pluripotency maintenance and lineage determination by utilizing efficient directed differentiation protocols. The results show loss-of-function of CHD8 does not affect human ESC maintenance although having slight effect on proliferation and cell cycle. Interestingly, CHD8 depletion results in defective neuroectoderm differentiation, along with severe cell death in neural progenitor stage. Transcriptome analysis also indicates CHD8 does not alter the expression of pluripotent genes in ESC stage, but in neural progenitor cells depletion of CHD8 induces the abnormal expression of the apoptosis genes and suppresses neuroectoderm-related genes. These results provide the evidence that CHD8 plays an essential role in the pluripotency exit and neuroectoderm differentiation as well as the regulation of apoptosis during neurogenesis.

| S-EPMC8536677 | biostudies-literature

Depletion of demethylase KDM6 enhances early neuroectoderm commitment of human ESCs through inhibiting WNT activation

Project description:Epigenetic modifications play a crucial role in learning, memory and neurogenesis, but the study of its role in early neuroectoderm commitment from pluripotent inner cell mass is relatively lack. Here we utilized the system of directed neuroectoderm differentiation from human embryonic stem cells and identified KDM6B, an enzyme responsible to erase H3K27me3, was the most upregulated enzyme of histone methylation during neuroectoderm differentiation by transcriptome analysis. We then constructed KDM6B-null embryonic stem cells and found strikingly, the cells with KDM6B knockout exhibited much higher neuroectoderm induction efficiency. Furthermore, we constructed a serial of embryonic stem cell lines knocking out the other H3K27 demethylase KDM6A, and depleting both KDM6A and KDM6B, respectively. These cell lines together confirmed KDM6 impeded early neuroectoderm commitment. By RNA-seq, we found a panel of WNT activation genes significantly downregulated while WNT inhibiting genes significantly upregulated upon depletion of KDM6. Functional rescue assayed that WNT agonist could abolish the differential neuroectoderm induction due to manipulating KDM6 demonstrated WNT was the major downstream of KDM6 during early neural induction. Taken together, our findings illustrated the important role of histone methylation modifier KDM6A and KDM6B in neuroectoderm differentiation and provided additional insights into the precise epigenetic regulation in different stage of neurogenesis.

2021-09-29 | GSE172312 | GEO

Chd8 mediates cortical neurogenesis through transcriptional regulation of cell cycle and Wnt signaling genes

Project description:De novo mutations in CHD8 are strongly associated with autism spectrum disorder (ASD), however the underlying mechanisms remain elusive. Here we report that Chd8 knockdown during cortical development results in defective neural progenitor proliferation and differentiation that ultimately manifests in abnormal neuronal morphology and behaviors in adult mice. Transcriptome analysis revealed that on the one hand Chd8 stimulates the transcription of cell cycle genes, while on the other it precludes the induction of neural specific genes by regulating the expression of PRC2 complex components. Furthermore, knockdown of Chd8 disrupts the expression of key transducers of Wnt signaling, and enhancing Wnt signaling rescues the transcriptional and behavioral deficits caused by Chd8 knockdown. We propose that these roles of Chd8 and the dynamics of its expression during development help negotiate the fine balance between neural progenitor proliferation and differentiation. Together, these observations provide new insights into the etiology of ASD.

2016-09-10 | GSE72442 | GEO

Role of Chd8 in Xist regulation

Project description:In this project, we have studied the role of Chd8 in Xist regulation and XCI initiation by means of Chd8 Knock-Downs (KD) and Knock-Out (KO).

2021-09-10 | PXD024155 | Pride

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

A dual functions of autism-related chromatin remodeler CHD8 in developmental and adult neurogenesis

Project description:The loss-of-function mutations in the chromatin remodeler CHD8, a high-risk factor in autism spectrum disorder (ASD), lead to severe developmental delay, however, the underlying mechanisms remains elusive. Here, we use transcriptome and genomic occupancy reveal that CHD8 regulates chromatin accessibility and activates neurogenesis-related genes for cortical neurogenesis.

2022-10-17 | GSE148608 | GEO

Genes differentially expressed upon CHD8 knockdown

2009-05-01 | GSE11422 | GEO

Depletion of demethylase KDM6 enhances early neuroectoderm commitment of human ESCs through inhibiting WNT activation

Project description:Depletion of demethylase KDM6 enhances early neuroectoderm commitment of human ESCs through inhibiting WNT activation

| PRJNA722914 | ENA

RNAseq data from ES and differentiated cells in Chd8 WT vs Chd8 KD and Chd8 KO cells

Project description:In this study, we compare the transcriptomic difference between WT and Chd8 depleted ES aand differentiating ES cells. We report significant differences between Chd8 WT and KD/KO cell lines.

2021-04-27 | GSE166858 | GEO

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