Evidence map›Paper›PMID 26274562›Full record

ArticleeLife2015

Down-regulation of TORC2-Ypk1 signaling promotes MAPK-independent survival under hyperosmotic stress.

Alexander Muir, Françoise M Roelants, Garrett Timmons, Kristin L Leskoske, Jeremy Thorner

Open access · goldAbstract read
In one paragraph

Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
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  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Phosphatidic acid biosynthesis in the model organism yeast Saccharomyces cerevisiae - a survey.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2021
    Review
  12. Plasma Membrane MCC/Eisosome Domains Promote Stress Resistance in Fungi.Microbiology and molecular biology reviews : MMBR · 2020
    Review
  13. Article
  14. Article
  15. Relevance and Regulation of Cell Density.Trends in cell biology · 2020
    Review
  16. Article
  17. Review
  18. Applied and environmental microbiology · 2019
    Article
  19. Article
  20. Article
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.

Alexander MuirDivision of Biochemistry, Biophysics and Structural Biology, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States.
Françoise M RoelantsDivision of Biochemistry, Biophysics and Structural Biology, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States.
Garrett TimmonsDepartment of Chemistry, University of California, Berkeley, Berkeley, United States.
Kristin L LeskoskeDivision of Biochemistry, Biophysics and Structural Biology, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States.
Jeremy ThornerDivision of Biochemistry, Biophysics and Structural Biology, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States.
University of California, Berkeley · US

Funding

THE MOLECULAR BASIS OF CELL FUNCTIONT32GM007232 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI BILDER, DAVID, UNAL, ELCIN · 1985 to 2022
$36.4M
Yeast Protein Kinase Signaling Networks: Specificity, Regulation and FunctionR01GM021841 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI THORNER, JEREMY W. · 1985 to 2019
$11.8M
NIGMS NIH HHS R01 GM021841NIGMS NIH HHS R01 GM21841NIGMS NIH HHS T32 GM007232NIGMS NIH HHS T32 GM07232
6 · The paper itself

Abstract

In eukaryotes, exposure to hypertonic conditions activates a MAPK (Hog1 in Saccharomyces cerevisiae and ortholog p38 in human cells). In yeast, intracellular glycerol accumulates to counterbalance the high external osmolarity. To prevent glycerol efflux, Hog1 action impedes the function of the aquaglyceroporin Fps1, in part, by displacing channel co-activators (Rgc1/2). However, Fps1 closes upon hyperosmotic shock even in hog1∆ cells, indicating another mechanism to prevent Fps1-mediated glycerol efflux. In our prior proteome-wide screen, Fps1 was identified as a target of TORC2-dependent protein kinase Ypk1 (Muir et al., 2014). We show here that Fps1 is an authentic Ypk1 substrate and that the open channel state of Fps1 requires phosphorylation by Ypk1. Moreover, hyperosmotic conditions block TORC2-dependent Ypk1-mediated Fps1 phosphorylation, causing channel closure, glycerol accumulation, and enhanced survival under hyperosmotic stress. These events are all Hog1-independent. Our findings define the underlying molecular basis of a new mechanism for responding to hypertonic conditions.

Indexed as

Osmotic PressureSignal TransductionDown-RegulationGene Expression Regulation, FungalGlycogen Synthase Kinase 3Mechanistic Target of Rapamycin Complex 2Membrane ProteinsMicrobial ViabilityMultiprotein ComplexesPhosphorylationProtein Processing, Post-TranslationalSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTOR Serine-Threonine KinasesFPS1 protein, S cerevisiaeGlycogen Synthase Kinase 3MCK1 protein, S cerevisiaeMechanistic Target of Rapamycin Complex 2Membrane ProteinsMultiprotein ComplexesSaccharomyces cerevisiae ProteinsTOR Serine-Threonine Kinasesaquaglyceroporinbiochemistrycell biologyosmosensingprotein kinaseS. cerevisiae

Identifiers

PMID26274562
PMCPMC4552222
OpenAlexW2128753174

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.