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EndoC-bH1 CRISPR Cas9

ABSTRACT: A CRISPR/Cas9 genome editing pipeline in the EndoC-βH1 cell line to study genes implicated in beta cell function

PROVIDER: PRJEB34547 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3549160.fastq.gz	Fastqsanger.gz
	ERR3549170.fastq.gz	Fastqsanger.gz
	ERR3549161.fastq.gz	Fastqsanger.gz
	ERR3549171.fastq.gz	Fastqsanger.gz
	ERR3549162.fastq.gz	Fastqsanger.gz

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Effect of deletion of ZHX3 on gene expression in human pancreatic beta cells EndoC-BH1

Project description:ZHX3 is a transcriptional factor whose role in human pancreatic beta cells is not well understood. In attempt to identify the genes that ZHX3 regulates in beta cells, we KO ZHX3 using CRISPR in EndoC-βH1 cells and performed RNA-Seq. We have only identified 36 and 31 genes that were significantly up and downregulated respectively. This is in concordance with our functional data whereby the KO of ZHX3 in EndoC-βH1 did not affect its insulin secretory function. Overall, we conclude that the KO of ZHX3 did not result in major perturbations in EndoC-βH1 cells.

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Project description:We have developped a novel human pancreatic beta cell line: EndoC-βH5. EndoC-βH5 cells are ready-to-use and storable cells with physiological insulin secretion. EndoC-βH5 cells were generated by integrative gene transfer of immortalizing transgenes hTERT and SV40 large T along with Herpes Simplex Virus-1 thymidine kinase into human fetal pancreas. Immortalizing transgenes were removed after amplification using CRE activation and remaining non-excized cells eliminated using ganciclovir. Resulting cells were distributed as ready to use EndoC-βH5 cells. We performed comparative transcriptome analysis with EndoC-βH1 cells , extensive functional and immunological assays. RNA-seq confirmed abundant expression of beta cell transcription factors and functional markers, including incretin receptors.

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Project description:EndoC-βH1 is emerging as a critical human β cell model to study the genetic and environmental etiologies of β cell (dys)function and diabetes. Comprehensive knowledge of its molecular landscape is lacking, yet required, for effective use of this model. Here, we report chromosomal (spectral karyotyping), genetic (genotyping), epigenomic (ChIP-seq and ATAC-seq), chromatin interaction (Hi-C and Pol2 ChIA-PET), and transcriptomic (RNA-seq and miRNA-seq) maps of EndoC-βH1. Analyses of these maps define known (e.g., PDX1 and ISL1) and putative (e.g., PCSK1 and mir-375) β cell-specific transcriptional cis-regulatory networks and identify allelic effects on cis-regulatory element use. Importantly, comparison with maps generated in primary human islets and/or β cells indicates preservation of chromatin looping but also highlights chromosomal aberrations and fetal genomic signatures in EndoC-βH1. Together, these maps, and a web application we created for their exploration, provide important tools for the design of experiments to probe and manipulate the genetic programs governing β cell identity and (dys)function in diabetes.

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