Evidence map›Paper›PMID 26232408›Full record

ArticleGenetics2015

Regulatory Rewiring in a Cross Causes Extensive Genetic Heterogeneity.

Takeshi Matsui, Robert Linder, Joann Phan, Fabian Seidl, Ian M Ehrenreich

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 13% of its field
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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. System drift and speciation.Evolution; international journal of organic evolution · 2022
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. The rewiring of transcription circuits in evolution.Current opinion in genetics & development · 2017
    Review
  8. Genetic suppression: Extending our knowledge from lab experiments to natural populations.BioEssays : news and reviews in molecular, cellular and developmental biology · 2017
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. 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

5 authors at 1 institution in 1 country.

Takeshi MatsuiMolecular and Computational Biology Section, Department of Biological Sciences, University of Southern California, Los Angeles, California 21546.
Robert LinderMolecular and Computational Biology Section, Department of Biological Sciences, University of Southern California, Los Angeles, California 21546.
Joann PhanMolecular and Computational Biology Section, Department of Biological Sciences, University of Southern California, Los Angeles, California 21546.
Fabian SeidlMolecular and Computational Biology Section, Department of Biological Sciences, University of Southern California, Los Angeles, California 21546.
Ian M EhrenreichMolecular and Computational Biology Section, Department of Biological Sciences, University of Southern California, Los Angeles, California 21546 ian.ehrenreich@usc.edu.
University of Southern California · US

Funding

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
NIAID NIH HHS R21 AI108939NIAID NIH HHS R21AI108939NIGMS NIH HHS R01 GM110255NIGMS NIH HHS R01GM110255
6 · The paper itself

Abstract

Genetic heterogeneity occurs when individuals express similar phenotypes as a result of different underlying mechanisms. Although such heterogeneity is known to be a potential source of unexplained heritability in genetic mapping studies, its prevalence and molecular basis are not fully understood. Here we show that substantial genetic heterogeneity underlies a model phenotype--the ability to grow invasively--in a cross of two Saccharomyces cerevisiae strains. The heterogeneous basis of this trait across genotypes and environments makes it difficult to detect causal loci with standard genetic mapping techniques. However, using selective genotyping in the original cross, as well as in targeted backcrosses, we detected four loci that contribute to differences in the ability to grow invasively. Identification of causal genes at these loci suggests that they act by changing the underlying regulatory architecture of invasion. We verified this point by deleting many of the known transcriptional activators of invasion, as well as the gene encoding the cell surface protein Flo11 from five relevant segregants and showing that these individuals differ in the genes they require for invasion. Our work illustrates the extensive genetic heterogeneity that can underlie a trait and suggests that regulatory rewiring is a basic mechanism that gives rise to this heterogeneity.

Indexed as

Genetic HeterogeneityChromosome MappingCrosses, GeneticGenotypeHumansMembrane GlycoproteinsPhenotypeQuantitative Trait LociSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsFLO11 protein, S cerevisiaeMembrane GlycoproteinsSaccharomyces cerevisiae Proteinscomplex traitsgenetic mappinginvasive growthregulatory networksyeast

Identifiers

PMID26232408
PMCPMC4596683
OpenAlexW2190686089

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.