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Identification of LZTFL1 as a candidate effector gene at a COVID-19 risk locus (ATAC-seq)

ABSTRACT: Identification of LZTFL1 as a candidate effector gene at a COVID-19 risk locus (ATAC-seq)

PROVIDER: PRJNA733669 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14685302_1.fastq.gz	Fastqsanger.gz
	SRR14685302_2.fastq.gz	Fastqsanger.gz
	SRR14685303_1.fastq.gz	Fastqsanger.gz
	SRR14685303_2.fastq.gz	Fastqsanger.gz
	SRR14685304_1.fastq.gz	Fastqsanger.gz

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Identification of LZTFL1 as a candidate effector gene at a COVID-19 risk locus

Project description:Identification of LZTFL1 as a candidate effector gene at a COVID-19 risk locus

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Identification of LZTFL1 as a candidate effector gene at a COVID-19 risk locus (ChIP-seq)

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Identification of LZTFL1 as a candidate effector gene at a COVID-19 risk locus

Project description:To identify a causative variant and effector gene responsible for a 2-fold increased risk of severe COVID-19, a multi-omics platform was deployed. A combination of ATAC-seq, ChIP-seq, Micro Capture-C and NuTi Capture-C were used to characterize a range of cell types, including epithelial, fibroblast, endothelial, immune and erythroid cells.

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Identification of LZTFL1 as a candidate effector gene at a COVID-19 risk locus (MCC)

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Project description:Individuals infected with the SARS-CoV-2 virus present with a wide variety of phenotypes ranging from asymptomatic to severe and even lethal outcomes. Past research has revealed a genetic haplotype on chromosome 3 that entered the human population via introgression from Neanderthals as the strongest genetic risk factor for the severe COVID-19 phenotype. However, the specific variants along this introgressed haplotype that contribute to this risk and the biological mechanisms that are involved remain unclear. Here, we assess the variants present on the risk haplotype for their likelihood of driving the severe COVID-19 phenotype. We do this by first exploring their impact on the regulation of genes involved in COVID-19 infection using a variety of population genetics and functional genomics tools. We then perform an locus-specific massively parallel reporter assay to individually assess the regulatory potential of each allele on the haplotype in a multipotent immune-related cell line. We ultimately reduce the set of over 600 linked genetic variants to identify 4 introgressed alleles that are strong functional candidates for driving the association between this locus and the severe COVID-19. These variants likely drive the locus’ impact on severity by putatively modulating the regulation of two critical chemokine receptor genes: CCR1 and CCR5. These alleles are ideal targets for future functional investigations into the interaction between host genomics and COVID-19 outcomes.

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Identification of LZTFL1 as a candidate effector gene at a COVID-19 risk locus (ChIP-seq)

Project description:To identify regulation by the CEBPB transcription factor in epithelial, fibroblast and endothelial cells ChIP-seq was carried out for both the transcription factor and marks of active transcription (H3K27ac).

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Identification of LZTFL1 as a candidate effector gene at a COVID-19 risk locus (ATAC-seq)

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Identification of LZTFL1 as a candidate effector gene at a COVID-19 risk locus.

Project description:The severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2) disease (COVID-19) pandemic has caused millions of deaths worldwide. Genome-wide association studies identified the 3p21.31 region as conferring a twofold increased risk of respiratory failure. Here, using a combined multiomics and machine learning approach, we identify the gain-of-function risk A allele of an SNP, rs17713054G>A, as a probable causative variant. We show with chromosome conformation capture and gene-expression analysis that the rs17713054-affected enhancer upregulates the interacting gene, leucine zipper transcription factor like 1 (LZTFL1). Selective spatial transcriptomic analysis of lung biopsies from patients with COVID-19 shows the presence of signals associated with epithelial-mesenchymal transition (EMT), a viral response pathway that is regulated by LZTFL1. We conclude that pulmonary epithelial cells undergoing EMT, rather than immune cells, are likely responsible for the 3p21.31-associated risk. Since the 3p21.31 effect is conferred by a gain-of-function, LZTFL1 may represent a therapeutic target.

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