SynthesisGenome biology and evolution2011
Genetic architecture of growth traits revealed by global epistatic interactions.
Synthesis in Genome biology and evolution, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
5 citing papers in PubMed.
- Bardet-Biedl syndrome: Genetics, molecular pathophysiology, and disease management.Indian journal of ophthalmology · 2016Review
- Dynamic epistasis under varying environmental perturbations.PloS one · 2015Article
- Genotype to phenotype maps: multiple input abiotic signals combine to produce growth effects via attenuating signaling interactions in maize.G3 (Bethesda, Md.) · 2013Article
- Predicting complex phenotype-genotype interactions to enable yeast engineering: Saccharomyces cerevisiae as a model organism and a cell factory.Biotechnology journal · 2013Review
- Predicting complex traits using a diffusion kernel on genetic markers with an application to dairy cattle and wheat data.Genetics, selection, evolution : GSE · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Epistasis has long been recognized as fundamentally important in understanding the structure, function, and evolutionary dynamics of biological systems. Yet, little is known about how it is distributed underlying specific traits. Based on a global map of epistatic interactions in baker's yeast, Saccharomyces cerevisiae, we show that epistasis is prevalent (∼13% increase from random expectation) and displays modular architecture among genes that underlie the same growth traits. More interestingly, our results indicate that hub genes responsible for the same growth traits tend to link epistatically with each other more frequently than random expectation. Our results provide a genome-wide perspective on the genetic architecture of growth traits in a eukaryotic organism.
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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.