Evidence map›Paper›PMID 30256697›Full record

ArticleMolecular biology of the cell2018

A constitutive active allele of the transcription factor Msn2 mimicking low PKA activity dictates metabolic remodeling in yeast.

Vera Pfanzagl, Wolfram Görner, Martin Radolf, Alexandra Parich, Rainer Schuhmacher, Joseph Strauss, Wolfgang Reiter, Christoph Schüller

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

13 citing papers in PubMed, 27 citations in OpenAlex.

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  6. Quiescence inAnnual review of genetics · 2022
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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

8 authors at 3 institutions in 1 country.

Vera PfanzaglDepartment of Chemistry, University of Natural Resources and Life Sciences, Vienna (BOKU), 1190 Vienna, Austria.
Wolfram GörnerDepartment for Biochemistry, Max. F. Perutz Laboratories, University of Vienna, 1030 Vienna, Austria.
Martin RadolfManagement Scientific Service/EHS, Research Institute of Molecular Pathology (IMP), 1030 Vienna, Austria.
Alexandra ParichDepartment of Agrobiotechnology (IFA-Tulln), Center for Analytical Chemistry, University of Natural Resources and Life Sciences, 3430 Tulln, Austria.
Rainer SchuhmacherDepartment of Agrobiotechnology (IFA-Tulln), Center for Analytical Chemistry, University of Natural Resources and Life Sciences, 3430 Tulln, Austria.
Joseph StraussDepartment of Chemistry, University of Natural Resources and Life Sciences, Vienna (BOKU), 1190 Vienna, Austria.
Wolfgang ReiterDepartment for Biochemistry, Max. F. Perutz Laboratories, University of Vienna, 1030 Vienna, Austria.
Christoph SchüllerDepartment of Applied Genetics and Cell Biology (DAGZ), University of Natural Resources and Life Sciences, 3430 Tulln, Austria.
BOKU University · ATMax Perutz Labs · ATResearch Institute of Molecular Pathology · AT

Funding

Austrian Science Fund FWF P 23355Austrian Science Fund FWF W 1224
6 · The paper itself

Abstract

In yeast, protein kinase A (PKA) adjusts transcriptional profiles, metabolic rates, and cell growth in accord with carbon source availability. PKA affects gene expression mostly via the transcription factors Msn2 and Msn4, two key regulators of the environmental stress response. Here we analyze the role of the PKA-Msn2 signaling module using an Msn2 allele that harbors serine-to-alanine substitutions at six functionally important PKA motifs (Msn2A6) . Expression of Msn2A6 mimics low PKA activity, entails a transcription profile similar to that of respiring cells, and prevents formation of colonies on glucose-containing medium. Furthermore, Msn2A6 leads to high oxygen consumption and hence high respiratory activity. Substantially increased intracellular concentrations of several carbon metabolites, such as trehalose, point to a metabolic adjustment similar to diauxic shift. This partial metabolic switch is the likely cause for the slow-growth phenotype in the presence of glucose. Consistently, Msn2A6 expression does not interfere with growth on ethanol and tolerated is to a limited degree in deletion mutant strains with a gene expression signature corresponding to nonfermentative growth. We propose that the lethality observed in mutants with hampered PKA activity resides in metabolic reprogramming that is initiated by Msn2 hyperactivity.

Indexed as

Cyclic AMPCyclic AMP-Dependent Protein KinasesDNA-Binding ProteinsGene FrequencyGlucosePhosphorylationPromoter Regions, GeneticResponse ElementsSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSignal TransductionTranscription FactorsTranscription, GeneticCyclic AMPCyclic AMP-Dependent Protein KinasesDNA-Binding ProteinsGlucoseMSN2 protein, S cerevisiaeMSN4 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsTranscription Factors

Identifiers

PMID30256697
PMCPMC6249869
OpenAlexW2892757564

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.