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Biology subjects

Largiader, C. R.

Publications and source records attributed to Largiader, C. R..

2 recordsLinked to original sources

Resolving the CES1 Genomic Locus with Cas9-Directed Targeted Long-Read Sequencing for Precision Pharmacogenomics

Carboxylesterase 1 (CES1) is the primary hepatic hydrolase in humans, crucial for the metabolism of ester-containing drugs and endogenous lipids. However, the CES1 genomic region is difficult to resolve because of adjacent highly homologous pseudogenes and the presence of large structural variants. These complexities often cause read misalignment and inaccurate variant calling with conventional short-read sequencing, hindering reliable pharmacogenomic analyses. To overcome these limitations, we employed an optimized, PCR-free Oxford Nanopore Technologies (ONT) sequencing method, Cas9directed targeted sequencing (nCATS), to characterize the targeted region of up to 76 kb, including CES1, CES1P1 or CES1A2, and their intergenic regions. This approach uses Cas9 to selectively enrich and sequence long native DNA fragments, while avoiding amplification-induced artefacts. Long-read sequencing was performed in 23 human blood samples and the HepG2 hepatoblastoma cell line enabling high-resolution mapping to the CES1 locus. We uncover five previously unrecognized main CES1 haplotypes and report that many single nucleotide variants (SNVs) in public databases are likely artefacts caused by short-read misalignment. Additionally, we identify long inverted repeats (LIRs) flanking a fragile genomic site within the region, which may form DNA hairpins and contribute to structural plasticity at the locus. This study demonstrates the utility of long-read sequencing for resolving complex genomic regions such as CES1, allowing comprehensive detection of structural variants and haplotype-resolved SNVs. Our findings provide improved reference sequences and deeper insight into CES1 diversity, with significant implications for future pharmacogenetic research and the development of personalized treatment strategies involving CES1-metabolized medications.

genetics↗

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↗