Evidence map›Paper›PMID 24784154›Full record

ArticlePLoS genetics2014

Genetic interactions involving five or more genes contribute to a complex trait in yeast.

Matthew B Taylor, Ian M Ehrenreich

Abstract read
In one paragraph

Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

54 citing papers in PubMed.

  1. Article
  2. Article
  3. Systematic data analysis pipeline for quantitative morphological cell phenotyping.Computational and structural biotechnology journal · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Regulatory role of Mss11 inFrontiers in cellular and infection microbiology · 2023
    Article
  8. Identification and Characterization of a QTL for Growth ofJournal of fungi (Basel, Switzerland) · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Genetic buffering and potentiation in metabolism.PLoS computational biology · 2020
    Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Matthew B TaylorMolecular and Computational Biology Section, Department of Biological Sciences, University of Southern California, Los Angeles, California, United States of America.
Ian M EhrenreichMolecular and Computational Biology Section, Department of Biological Sciences, University of Southern California, Los Angeles, California, United States of America.

Funding

Implications of haplotype structure in the human genomeP50HG002790 · NHGRI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI TAVARE, SIMON · 2003 to 2013
$29.9M
Comprehensive dissection of higher-order genetic interactionsR01GM110255 · NIGMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI EHRENREICH, IAN MICHAEL · 2014 to 2018
$1.4M
Genetic basis and pathogenicity of invasive growth in yeastR21AI108939 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI EHRENREICH, IAN MICHAEL · 2014 to 2015
$439k
NHGRI NIH HHS P50 HG002790NHGRI NIH HHS P50HG002790NIAID NIH HHS R21 AI108939NIAID NIH HHS R21AI108939NIGMS NIH HHS R01 GM110255
6 · The paper itself

Abstract

Recent research suggests that genetic interactions involving more than two loci may influence a number of complex traits. How these 'higher-order' interactions arise at the genetic and molecular levels remains an open question. To provide insights into this problem, we dissected a colony morphology phenotype that segregates in a yeast cross and results from synthetic higher-order interactions. Using backcrossing and selective sequencing of progeny, we found five loci that collectively produce the trait. We fine-mapped these loci to 22 genes in total and identified a single gene at each locus that caused loss of the phenotype when deleted. Complementation tests or allele replacements provided support for functional variation in these genes, and revealed that pre-existing genetic variants and a spontaneous mutation interact to cause the trait. The causal genes have diverse functions in endocytosis (END3), oxidative stress response (TRR1), RAS-cAMP signalling (IRA2), and transcriptional regulation of multicellular growth (FLO8 and MSS11), and for the most part have not previously been shown to exhibit functional relationships. Further efforts uncovered two additional loci that together can complement the non-causal allele of END3, suggesting that multiple genotypes in the cross can specify the same phenotype. Our work sheds light on the complex genetic and molecular architecture of higher-order interactions, and raises questions about the broader contribution of such interactions to heritable trait variation.

Indexed as

Genes, FungalChromosomes, FungalSaccharomyces cerevisiaeSelection, Genetic

Identifiers

PMID24784154
PMCPMC4006734

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.