Evidence map›Paper›PMID 25569670›Full record

ArticlePLoS genetics2015

Genetic mapping of MAPK-mediated complex traits Across S. cerevisiae.

Sebastian Treusch, Frank W Albert, Joshua S Bloom, Iulia E Kotenko, Leonid Kruglyak

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.2field-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

31 citing papers in PubMed, 63 citations in OpenAlex.

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  18. Genetics ofeLife · 2018
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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 2 institutions in 1 country.

Sebastian TreuschLewis Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey, United States of America.
Frank W AlbertDepartment of Human Genetics, University of California, Los Angeles, Los Angeles, California, United States of America.
Joshua S BloomHoward Hughes Medical Institute, Department of Human Genetics, University of California, Los Angeles, Los Angeles, California, United States of America.
Iulia E KotenkoLewis Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey, United States of America.
Leonid KruglyakHoward Hughes Medical Institute, Department of Human Genetics, University of California, Los Angeles, Los Angeles, California, United States of America; Howard Hughes Medical Institute, Department of Biological Chemistry, University of California, Los Angeles, Los Angeles, California, United States of America.
University of California, Los Angeles · USPrinceton University · US

Funding

Toward comprehensive genetic dissection of complex traits in yeastR01GM102308 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LEONID KRUGLYAK · 2012 to 2026
$3.3M
Influence of genetic variation on fungal MAPK signaling and virulenceF32GM101857 · NIGMS · PRINCETON UNIVERSITY · PI TREUSCH, SEBASTIAN · 2012 to 2014
$117k
NIGMS NIH HHS F32 GM101857NIGMS NIH HHS F32 GM101857-02NIGMS NIH HHS R01 GM102308NIGMS NIH HHS R01GM102308
6 · The paper itself

Abstract

Signaling pathways enable cells to sense and respond to their environment. Many cellular signaling strategies are conserved from fungi to humans, yet their activity and phenotypic consequences can vary extensively among individuals within a species. A systematic assessment of the impact of naturally occurring genetic variation on signaling pathways remains to be conducted. In S. cerevisiae, both response and resistance to stressors that activate signaling pathways differ between diverse isolates. Here, we present a quantitative trait locus (QTL) mapping approach that enables us to identify genetic variants underlying such phenotypic differences across the genetic and phenotypic diversity of S. cerevisiae. Using a Round-robin cross between twelve diverse strains, we identified QTL that influence phenotypes critically dependent on MAPK signaling cascades. Genetic variants under these QTL fall within MAPK signaling networks themselves as well as other interconnected signaling pathways. Finally, we demonstrate how the mapping results from multiple strain background can be leveraged to narrow the search space of causal genetic variants.

Indexed as

Chromosome MappingGenotypeMitogen-Activated Protein Kinase KinasesPhenotypePolymorphism, Single NucleotideQuantitative Trait LociSaccharomyces cerevisiaeSignal TransductionMitogen-Activated Protein Kinase Kinases

Identifiers

PMID25569670
PMCPMC4287466
OpenAlexW2028772908

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.