ArticleNature communications2023
eQTL mapping in fetal-like pancreatic progenitor cells reveals early developmental insights into diabetes risk.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 19 citations in OpenAlex.
- Multiomic QTL mapping reveals phenotypic complexity of GWAS loci and prioritizes putative causal variants.Cell genomics · 2025Article
- Cell type and dynamic state govern genetic regulation of gene expression in heterogeneous differentiating cultures.Cell genomics · 2024Article
- Multi-omics characterization of type 2 diabetes associated genetic variation.medRxiv : the preprint server for health sciences · 2024Article
- Integrated mendelian randomization analyses highlight AFF3 as a novel eQTL-mediated susceptibility gene in renal cancer and its potential mechanisms.BMC cancer · 2024Article
- Complex regulatory networks influence pluripotent cell state transitions in human iPSCs.Nature communications · 2024Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
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Abstract
The impact of genetic regulatory variation active in early pancreatic development on adult pancreatic disease and traits is not well understood. Here, we generate a panel of 107 fetal-like iPSC-derived pancreatic progenitor cells (iPSC-PPCs) from whole genome-sequenced individuals and identify 4065 genes and 4016 isoforms whose expression and/or alternative splicing are affected by regulatory variation. We integrate eQTLs identified in adult islets and whole pancreas samples, which reveal 1805 eQTL associations that are unique to the fetal-like iPSC-PPCs and 1043 eQTLs that exhibit regulatory plasticity across the fetal-like and adult pancreas tissues. Colocalization with GWAS risk loci for pancreatic diseases and traits show that some putative causal regulatory variants are active only in the fetal-like iPSC-PPCs and likely influence disease by modulating expression of disease-associated genes in early development, while others with regulatory plasticity likely exert their effects in both the fetal and adult pancreas by modulating expression of different disease genes in the two developmental stages.
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