ArticlePLoS genetics2017
Widespread epistasis regulates glucose homeostasis and gene expression.
Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed.
- Concordance between male- and female-specific GWAS results helps define underlying genetic architecture of complex traits.Nature communications · 2025Article
- Epistatic contributions to human traits via transcription factor mechanisms.medRxiv : the preprint server for health sciences · 2025Article
- Mapping of genotype-by-environment interaction loci for Metabolic Syndrome-like traits using the multi-parentbioRxiv : the preprint server for biology · 2025Article
- The impact of species-wide gene expression variation on Caenorhabditis elegans complex traits.Nature communications · 2022Article
- Prediction performance of linear models and gradient boosting machine on complex phenotypes in outbred mice.G3 (Bethesda, Md.) · 2022Article
- Article
- A model and test for coordinated polygenic epistasis in complex traits.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- A Novel Mapping Strategy Utilizing Mouse Chromosome Substitution Strains Identifies Multiple Epistatic Interactions That Regulate Complex Traits.G3 (Bethesda, Md.) · 2020Article
- Discovering Genetic Factors for psoriasis through exhaustively searching for significant second order SNP-SNP interactions.Scientific reports · 2018Article
- Epigenetic control of variation and stochasticity in metabolic disease.Molecular metabolism · 2018Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
The relative contributions of additive versus non-additive interactions in the regulation of complex traits remains controversial. This may be in part because large-scale epistasis has traditionally been difficult to detect in complex, multi-cellular organisms. We hypothesized that it would be easier to detect interactions using mouse chromosome substitution strains that simultaneously incorporate allelic variation in many genes on a controlled genetic background. Analyzing metabolic traits and gene expression levels in the offspring of a series of crosses between mouse chromosome substitution strains demonstrated that inter-chromosomal epistasis was a dominant feature of these complex traits. Epistasis typically accounted for a larger proportion of the heritable effects than those due solely to additive effects. These epistatic interactions typically resulted in trait values returning to the levels of the parental CSS host strain. Due to the large epistatic effects, analyses that did not account for interactions consistently underestimated the true effect sizes due to allelic variation or failed to detect the loci controlling trait variation. These studies demonstrate that epistatic interactions are a common feature of complex traits and thus identifying these interactions is key to understanding their genetic regulation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.