DNA-binding factor footprints and enhancer RNAs identify functional non-coding genetic variants.

Functional genetics Functional genomics Genome-wide association study Non-coding genome Non-coding variants Single nucleotide polymorphism Single nucleotide variants

Journal

Genome biology
ISSN: 1474-760X
Titre abrégé: Genome Biol
Pays: England
ID NLM: 100960660

Informations de publication

Date de publication:
06 Aug 2024
Historique:
received: 06 03 2024
accepted: 25 07 2024
medline: 7 8 2024
pubmed: 7 8 2024
entrez: 6 8 2024
Statut: epublish

Résumé

Genome-wide association studies (GWAS) have revealed a multitude of candidate genetic variants affecting the risk of developing complex traits and diseases. However, the highlighted regions are typically in the non-coding genome, and uncovering the functional causative single nucleotide variants (SNVs) is challenging. Prioritization of variants is commonly based on genomic annotation with markers of active regulatory elements, but current approaches still poorly predict functional variants. To address this, we systematically analyze six markers of active regulatory elements for their ability to identify functional variants. We benchmark against molecular quantitative trait loci (molQTL) from assays of regulatory element activity that identify allelic effects on DNA-binding factor occupancy, reporter assay expression, and chromatin accessibility. We identify the combination of DNase footprints and divergent enhancer RNA (eRNA) as markers for functional variants. This signature provides high precision, but with a trade-off of low recall, thus substantially reducing candidate variant sets to prioritize variants for functional validation. We present this as a framework called FINDER-Functional SNV IdeNtification using DNase footprints and eRNA. We demonstrate the utility to prioritize variants using leukocyte count trait and analyze variants in linkage disequilibrium with a lead variant to predict a functional variant in asthma. Our findings have implications for prioritizing variants from GWAS, in development of predictive scoring algorithms, and for functionally informed fine mapping approaches.

Sections du résumé

BACKGROUND BACKGROUND
Genome-wide association studies (GWAS) have revealed a multitude of candidate genetic variants affecting the risk of developing complex traits and diseases. However, the highlighted regions are typically in the non-coding genome, and uncovering the functional causative single nucleotide variants (SNVs) is challenging. Prioritization of variants is commonly based on genomic annotation with markers of active regulatory elements, but current approaches still poorly predict functional variants. To address this, we systematically analyze six markers of active regulatory elements for their ability to identify functional variants.
RESULTS RESULTS
We benchmark against molecular quantitative trait loci (molQTL) from assays of regulatory element activity that identify allelic effects on DNA-binding factor occupancy, reporter assay expression, and chromatin accessibility. We identify the combination of DNase footprints and divergent enhancer RNA (eRNA) as markers for functional variants. This signature provides high precision, but with a trade-off of low recall, thus substantially reducing candidate variant sets to prioritize variants for functional validation. We present this as a framework called FINDER-Functional SNV IdeNtification using DNase footprints and eRNA.
CONCLUSIONS CONCLUSIONS
We demonstrate the utility to prioritize variants using leukocyte count trait and analyze variants in linkage disequilibrium with a lead variant to predict a functional variant in asthma. Our findings have implications for prioritizing variants from GWAS, in development of predictive scoring algorithms, and for functionally informed fine mapping approaches.

Identifiants

pubmed: 39107801
doi: 10.1186/s13059-024-03352-1
pii: 10.1186/s13059-024-03352-1
doi:

Substances chimiques

DNA-Binding Proteins 0
Enhancer RNAs 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

208

Subventions

Organisme : Medical Research Council
ID : MC_UU_00007/2
Pays : United Kingdom
Organisme : Chief Scientist Office, Scottish Government Health and Social Care Directorate
ID : PCL/20/02
Organisme : Swiss National Science Foundation
ID : P500PB_206805
Pays : Switzerland

Informations de copyright

© 2024. The Author(s).

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Auteurs

Simon C Biddie (SC)

MRC Human Genetics Unit, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK. Simon.Biddie@ed.ac.uk.
NHS Lothian, Edinburgh, UK. Simon.Biddie@ed.ac.uk.

Giovanna Weykopf (G)

MRC Human Genetics Unit, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK.

Elizabeth F Hird (EF)

NHS Lothian, Edinburgh, UK.

Elias T Friman (ET)

MRC Human Genetics Unit, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK.

Wendy A Bickmore (WA)

MRC Human Genetics Unit, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK. Wendy.Bickmore@ed.ac.uk.

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