Search bioRxiv⌕ Search

Biology subjects

Etheridge, A. S.

Publications and source records attributed to Etheridge, A. S..

2 recordsLinked to original sources

Liver single-nucleus multiome profiling reveals cell-type mechanisms for cardiometabolic traits

The liver is a central regulator of cardiometabolic physiology, coordinating processes such as lipid and glucose metabolism, protein synthesis, and detoxification. Genome-wide association studies (GWAS) have identified hundreds of genetic variants associated with cardiometabolic traits, yet their molecular mechanisms in liver cell types remain unclear. Using multiome single-nucleus RNA and ATAC sequencing on liver samples from 39 individuals, we profiled gene expression and chromatin accessibility in 68,398 nuclei across six primary liver cell types. We identified 306,706 accessible chromatin regions, including 70,884 regions undetected in bulk tissue analyses and that predominantly represent less abundant cell types. To identify genetic effects on gene regulation in liver cell types, we mapped quantitative trait loci (QTLs) and detected 1,885 chromatin accessibility QTLs (caQTLs) and 67 expression QTLs (eQTLs). We integrated cell-type QTLs with GWAS signals and revealed cell types, genes, and chromatin regulatory elements involved in cardiometabolic traits, such as liver enzyme and cholesterol levels. Non-hepatocyte cell-type QTL analyses exposed previously obscured mechanisms, such as an eQTL for ADAMTS12 in liver sinusoidal endothelial cells potentially involved in liver fibrosis, demonstrating that single-nucleus approaches can capture regulatory events missed in bulk analyses. Furthermore, we predicted cell type of action for bulk liver caQTLs colocalized with GWAS signals, enhancing mechanistic insights for complex trait associations. Our findings provide a high-resolution map of the hepatic regulatory landscape and advance the understanding of cellular contexts and molecular mechanisms underlying cardiometabolic traits.

genomics↗

Germline cis variant determines epigenetic regulation of the anti-cancer drug metabolism gene dihydropyrimidine dehydrogenase (DPYD)

Enhancers are critical for regulating tissue-specific gene expression, and genetic variants within enhancer regions have been suggested to contribute to various cancer-related processes, including therapeutic resistance. However, the precise mechanisms remain elusive. Using a well-defined drug-gene pair, we identified an enhancer region for dihydropyrimidine dehydrogenase (DPD, DPYD gene) expression that is relevant to the metabolism of the anti-cancer drug 5-fluorouracil (5-FU). Using reporter systems, CRISPR genome edited cell models, and human liver specimens, we demonstrated in vitro and vivo that genotype status for the common germline variant (rs4294451; 27% global minor allele frequency) located within this novel enhancer controls DPYD transcription and alters resistance to 5-FU. The variant genotype increases recruitment of the transcription factor CEBPB to the enhancer and alters the level of direct interactions between the enhancer and DPYD promoter. Our data provide insight into the regulatory mechanisms controlling sensitivity and resistance to 5-FU.

pharmacology and toxicology↗