Evidence map›Paper›PMID 32470059›Full record

ArticlePloS one2020

A tps1Δ persister-like state in Saccharomyces cerevisiae is regulated by MKT1.

Patrick A Gibney, Anqi Chen, Ariel Schieler, Jonathan C Chen, Yifan Xu, David G Hendrickson, R Scott McIsaac, Joshua D Rabinowitz, David Botstein

Abstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Disruption ofmicroPublication biology · 2023
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  3. Article
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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

9 authors.

Patrick A GibneyLewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey, United States of America.ORCID 0000-0003-1392-7553
Anqi ChenDepartment of Food Science, Cornell University, Ithaca, New York, United States of America.
Ariel SchielerLewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey, United States of America.
Jonathan C ChenLewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey, United States of America.ORCID 0000-0003-4346-0501
Yifan XuLewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey, United States of America.
David G HendricksonCalico Life Sciences LLC, South San Francisco, California, United States of America.
R Scott McIsaacCalico Life Sciences LLC, South San Francisco, California, United States of America.
Joshua D RabinowitzLewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey, United States of America.
David BotsteinLewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey, United States of America.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Trehalose metabolism in yeast has been linked to a variety of phenotypes, including heat resistance, desiccation tolerance, carbon-source utilization, and sporulation. The relationships among the several phenotypes of mutants unable to synthesize trehalose are not understood, even though the pathway is highly conserved. One of these phenotypes is that tps1Δ strains cannot reportedly grow on media containing glucose or fructose, even when another carbon source they can use (e.g. galactose) is present. Here we corroborate the recent observation that a small fraction of yeast tps1Δ cells do grow on glucose, unlike the majority of the population. This is not due to a genetic alteration, but instead resembles the persister phenotype documented in many microorganisms and cancer cells undergoing lethal stress. We extend these observations to show that this phenomenon is glucose-specific, as it does not occur on another highly fermented carbon source, fructose. We further demonstrate that this phenomenon appears to be related to mitochondrial complex III function, but unrelated to inorganic phosphate levels in the cell, as had previously been suggested. Finally, we found that this phenomenon is specific to S288C-derived strains, and is the consequence of a variant in the MKT1 gene.

Indexed as

Electron Transport Complex IIIFermentationFructoseGlucoseGlucosyltransferasesLoss of Function MutationSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTrehaloseElectron Transport Complex IIIFructoseGlucoseGlucosyltransferasesMKT1 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsTrehalosetrehalose-6-phosphate synthase

Identifiers

PMID32470059
PMCPMC7259636

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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.