Evidence map›Paper›PMID 36350693›Full record

ArticleeLife2022

Modeling single-cell phenotypes links yeast stress acclimation to transcriptional repression and pre-stress cellular states.

Andrew C Bergen, Rachel A Kocik, James Hose, Megan N McClean, Audrey P Gasch

Open access · goldAbstract read
In one paragraph

Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

10 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Dynamic phosphorylation of Hcm1 promotes fitness in chronic stress.bioRxiv : the preprint server for biology · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Advances inJournal of fungi (Basel, Switzerland) · 2023
    Review
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.

Andrew C Bergen *Center for Genomic Science Innovation, University of Wisconsin-Madison, Madison, United States.ORCID 0000-0003-1295-7718
Rachel A Kocik *Center for Genomic Science Innovation, University of Wisconsin-Madison, Madison, United States.ORCID 0000-0003-2422-4538
James HoseCenter for Genomic Science Innovation, University of Wisconsin-Madison, Madison, United States.
Megan N McCleanCenter for Genomic Science Innovation, University of Wisconsin-Madison, Madison, United States.
Audrey P GaschCenter for Genomic Science Innovation, University of Wisconsin-Madison, Madison, United States.ORCID 0000-0002-8182-257X
University of Wisconsin–Madison · US

Funding

Elucidating the network design principles of biological signal processingR35GM128873 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI Megan N McClean · 2018 to 2026
$4.0M
Molecular approaches to sensitizing eukaryotic cells to aneuploidyR01CA229532 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI GASCH, AUDREY · 2018 to 2022
$1.8M
NCI NIH HHS R01 CA229532NIGMS NIH HHS R35 GM128873
6 · The paper itself

Abstract

Stress defense and cell growth are inversely related in bulk culture analyses; however, these studies miss substantial cell-to-cell heterogeneity, thus obscuring true phenotypic relationships. Here, we devised a microfluidics system to characterize multiple phenotypes in single yeast cells over time before, during, and after salt stress. The system measured cell and colony size, growth rate, and cell-cycle phase along with nuclear trans-localization of two transcription factors: stress-activated Msn2 that regulates defense genes and Dot6 that represses ribosome biogenesis genes during an active stress response. By tracking cells dynamically, we discovered unexpected discordance between Msn2 and Dot6 behavior that revealed subpopulations of cells with distinct growth properties. Surprisingly, post-stress growth recovery was positively corelated with activation of the Dot6 repressor. In contrast, cells lacking Dot6 displayed slower growth acclimation, even though they grow normally in the absence of stress. We show that wild-type cells with a larger Dot6 response display faster production of Msn2-regulated Ctt1 protein, separable from the contribution of Msn2. These results are consistent with the model that transcriptional repression during acute stress in yeast provides a protective response, likely by redirecting translational capacity to induced transcripts.

Indexed as

Saccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsAcclimatizationDNA-Binding ProteinsGene Expression Regulation, FungalPhenotypeRepressor ProteinsTranscription FactorsDNA-Binding ProteinsDot6 protein, S cerevisiaeMSN2 protein, S cerevisiaeRepressor ProteinsSaccharomyces cerevisiae ProteinsTranscription Factorscell biologycell signalingfitnessheterogeneityS. cerevisiaestress responseyeast

Identifiers

PMID36350693
PMCPMC9678356
OpenAlexW4308608888

What Socratic 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 Socratic graph.