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Cell-type-specific and disease-associated expression quantitative trait loci in the human lung

Heini M. Natri, Christina B. Azodi, Lance Peter, Chase J. Taylor, Sagrika Chugh, Robert Kendle, Mei-I Chung, David K. Flaherty, Brittany K. Matlock, Carla L. Calvi, Timothy S. Blackwell, Lorraine B. Ware, Matthew Bacchetta, Rajat Walia, Ciara M. Shaver, Jonathan A. Kropski, Davis J. McCarthy, Nicholas E. Banovich

2024Nature Genetics92 citationsDOIOpen Access PDF

Abstract

Common genetic variants confer substantial risk for chronic lung diseases, including pulmonary fibrosis. Defining the genetic control of gene expression in a cell-type-specific and context-dependent manner is critical for understanding the mechanisms through which genetic variation influences complex traits and disease pathobiology. To this end, we performed single-cell RNA sequencing of lung tissue from 66 individuals with pulmonary fibrosis and 48 unaffected donors. Using a pseudobulk approach, we mapped expression quantitative trait loci (eQTLs) across 38 cell types, observing both shared and cell-type-specific regulatory effects. Furthermore, we identified disease interaction eQTLs and demonstrated that this class of associations is more likely to be cell-type-specific and linked to cellular dysregulation in pulmonary fibrosis. Finally, we connected lung disease risk variants to their regulatory targets in disease-relevant cell types. These results indicate that cellular context determines the impact of genetic variation on gene expression and implicates context-specific eQTLs as key regulators of lung homeostasis and disease.

Topics & Concepts

BiologyExpression quantitative trait lociCell typeContext (archaeology)Quantitative trait locusPulmonary fibrosisGenome-wide association studyGeneticsDiseaseGeneRegulation of gene expressionCellGene expressionLungGenotypeSingle-nucleotide polymorphismPathologyInternal medicineMedicinePaleontologyInterstitial Lung Diseases and Idiopathic Pulmonary FibrosisChronic Obstructive Pulmonary Disease (COPD) ResearchIL-33, ST2, and ILC Pathways
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