Evidence map›Paper›PMID 22102822›Full record

ArticlePLoS genetics2011

Multiple means to the same end: the genetic basis of acquired stress resistance in yeast.

David B Berry, Qiaoning Guan, James Hose, Suraiya Haroon, Marinella Gebbia, Lawrence E Heisler, Corey Nislow, Guri Giaever, Audrey P Gasch

Abstract read
In one paragraph

Article in PLoS genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing 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

64 citing papers in PubMed.

  1. Review
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  5. Surprising regulatory plasticity for the conserved HOG pathway in diversebioRxiv : the preprint server for biology · 2025
    Article
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  16. A rate threshold mechanism regulates MAPK stress signaling and survival.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  17. Article
  18. Article
  19. Article
  20. Article

4 more citing papers are in PubMed but not listed here.

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

9 authors.

David B BerryLaboratory of Genetics, University of Wisconsin-Madison, Madison, Wisconsin, United States of America.
Qiaoning Guan
James Hose
Suraiya Haroon
Marinella Gebbia
Lawrence E Heisler
Corey Nislow
Guri Giaever
Audrey P Gasch

Funding

PREDOCTORAL TRAINING PROGRAM IN GENETICST32GM007133 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI PERNA, NICOLE T · 1985 to 2023
$16.5M
Functional Genomics of Stress Defense in YeastR01GM083989 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI GASCH, AUDREY · 2008 to 2016
$3.0M
CIHR 84305CIHR MOP-81340NIGMS NIH HHS 5T32GM07133NIGMS NIH HHS R01 GM083989NIGMS NIH HHS T32 GM007133
6 · The paper itself

Abstract

In nature, stressful environments often occur in combination or close succession, and thus the ability to prepare for impending stress likely provides a significant fitness advantage. Organisms exposed to a mild dose of stress can become tolerant to what would otherwise be a lethal dose of subsequent stress; however, the mechanism of this acquired stress tolerance is poorly understood. To explore this, we exposed the yeast gene-deletion libraries, which interrogate all essential and non-essential genes, to successive stress treatments and identified genes necessary for acquiring subsequent stress resistance. Cells were exposed to one of three different mild stress pretreatments (salt, DTT, or heat shock) and then challenged with a severe dose of hydrogen peroxide (H(2)O(2)). Surprisingly, there was little overlap in the genes required for acquisition of H(2)O(2) tolerance after different mild-stress pretreatments, revealing distinct mechanisms of surviving H(2)O(2) in each case. Integrative network analysis of these results with respect to protein-protein interactions, synthetic-genetic interactions, and functional annotations identified many processes not previously linked to H(2)O(2) tolerance. We tested and present several models that explain the lack of overlap in genes required for H(2)O(2) tolerance after each of the three pretreatments. Together, this work shows that acquired tolerance to the same severe stress occurs by different mechanisms depending on prior cellular experiences, underscoring the context-dependent nature of stress tolerance.

Indexed as

Gene ExpressionGene Regulatory NetworksGenetic FitnessHeat-Shock ProteinsHeat-Shock ResponseHot TemperatureHydrogen PeroxideMultilocus Sequence TypingOligonucleotide Array Sequence AnalysisOxidative StressSaccharomyces cerevisiaeSodium ChlorideStress, PhysiologicalHeat-Shock ProteinsHydrogen PeroxideSodium Chloride

Identifiers

PMID22102822
PMCPMC3213159

What OpenQuestion holds

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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.