Evidence map›Paper›PMID 27248513›Full record

ArticleNature communications2016

Diverse genetic architectures lead to the same cryptic phenotype in a yeast cross.

Matthew B Taylor, Joann Phan, Jonathan T Lee, Madelyn McCadden, Ian M Ehrenreich

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

24 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
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  15. Review
  16. Genetic suppression: Extending our knowledge from lab experiments to natural populations.BioEssays : news and reviews in molecular, cellular and developmental biology · 2017
    Review
  17. Article
  18. Review
  19. Article
  20. G3 (Bethesda, Md.) · 2017
    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.

Matthew B TaylorMolecular and Computational Biology Section, Department of Biological Sciences, University of Southern California, Los Angeles, California 90089, USA.
Joann PhanMolecular and Computational Biology Section, Department of Biological Sciences, University of Southern California, Los Angeles, California 90089, USA.
Jonathan T LeeMolecular and Computational Biology Section, Department of Biological Sciences, University of Southern California, Los Angeles, California 90089, USA.
Madelyn McCaddenMolecular and Computational Biology Section, Department of Biological Sciences, University of Southern California, Los Angeles, California 90089, USA.
Ian M EhrenreichMolecular and Computational Biology Section, Department of Biological Sciences, University of Southern California, Los Angeles, California 90089, USA.
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 AI108939NIGMS NIH HHS R01 GM110255
6 · The paper itself

Abstract

Cryptic genetic variants that do not typically influence traits can interact epistatically with each other and mutations to cause unexpected phenotypes. To improve understanding of the genetic architectures and molecular mechanisms that underlie these interactions, we comprehensively dissected the genetic bases of 17 independent instances of the same cryptic colony phenotype in a yeast cross. In eight cases, the phenotype resulted from a genetic interaction between a de novo mutation and one or more cryptic variants. The number and identities of detected cryptic variants depended on the mutated gene. In the nine remaining cases, the phenotype arose without a de novo mutation due to two different classes of higher-order genetic interactions that only involve cryptic variants. Our results may be relevant to other species and disease, as most of the mutations and cryptic variants identified in our study reside in components of a partially conserved and oncogenic signalling pathway.

Indexed as

Epistasis, GeneticGene Expression Regulation, FungalGenome, FungalChromosome MappingConserved SequenceCrosses, GeneticFungal ProteinsGenotypeMutationOncogene ProteinsPhenotypeSaccharomyces cerevisiaeSignal TransductionFungal ProteinsOncogene Proteins

Identifiers

PMID27248513
PMCPMC4895441
OpenAlexW2408929192

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.