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Genome-wide CRISPR screening identifies SEC31A as a regulator of alpha cell survival

ABSTRACT: Genome-wide CRISPR screening identifies SEC31A as a regulator of alpha cell survival

PROVIDER: PRJNA917308 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22950320_1.fastq.gz	Fastqsanger.gz
	SRR22950320_2.fastq.gz	Fastqsanger.gz
	SRR22950321_1.fastq.gz	Fastqsanger.gz
	SRR22950321_2.fastq.gz	Fastqsanger.gz
	SRR22950322_1.fastq.gz	Fastqsanger.gz

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Genome-wide CRISPR screening identifies SEC31A as a regulator of alpha cell survival

Project description:Impairment of the glucagon response to hypoglycemia is among the severe clinical consequences in patients with type 1 or advanced type 2 diabetes. However, an incomplete understanding of the stress-response mechanism(s) in alpha cells has limited the insights into the pathophysiology underlying the dysregulated glucagon response and precluded the development of therapeutics. In this study, we undertook an unbiased, genome-wide screening by transducing alpha cells with a CRISPR lentiviral library to identify potential proteins that regulate stress resistance in alpha cells. We identified SEC31A, a gene responsible for the ER-Golgi transportation system, as a critical mediator of cell survival in response to stress. To provide clinical relevance to these findings, we performed transcriptome analysis using pseudoislets generated from sorted and re-aggregated human alpha cells with a knockdown of SEC31A. Our study offers insights into the regulatory mechanism(s) underlying ER stress resistance in pancreatic alpha cells with implications for treating hypoglycemia in T1D and advanced T2D

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