Evidence map›Paper›PMID 20388713›Full record

ArticleThe Journal of biological chemistry2010

Mtl1 is required to activate general stress response through Tor1 and Ras2 inhibition under conditions of glucose starvation and oxidative stress.

Mima Ivanova Petkova, Nuria Pujol-Carrion, Javier Arroyo, Jesús García-Cantalejo, Maria Angeles de la Torre-Ruiz

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 13% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

  1. Pooled it
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  9. Comparative Proteomics Analysis Reveals Unique Early Signaling Response ofInternational journal of molecular sciences · 2020
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  12. Integrins in disguise - mechanosensors inMicrobial cell (Graz, Austria) · 2019
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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

5 authors at 3 institutions in 1 country.

Mima Ivanova PetkovaDepartament de Ciències Mèdiques Bàsiques-IRBLleida, Facultad de Medicina, Universidad de Lleida, Lleida 25008, Spain.
Nuria Pujol-Carrion
Javier Arroyo
Jesús García-Cantalejo
Maria Angeles de la Torre-Ruiz
Universidad Complutense de Madrid · ESUniversitat de Lleida · ESBiomedical Research Institute of Lleida · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mtl1 is a member of the cell wall integrity (CWI) pathway of Saccharomyces cerevisiae, which functions as a cell wall sensor for oxidative stress. Genome-wide transcriptional analysis revealed a cluster of genes that were down-regulated in the absence of Mtl1. Many of these genes were potentially regulated by the general stress response factor Msn2/Msn4. In response to rapamycin, caffeine, glucose starvation and oxidative stress provoked by H(2)O(2), mtl1 presents a significant loss of viability as well as a deficiency in the transcriptional response mediated by Msn2/Msn4. The Mtl1 function was required (i) to induce ribosomal gene repression, (ii) to induce the general stress response driven by the transcription factor Msn2/Msn4, and (iii) to activate the CWI pathway in response to both glucose starvation and oxidative stress. We also detected higher cAMP levels in the mtl1 mutant than in wild type cells indicative of up-regulated RAS2-PKA activity. Disruption of TOR1, disruption of RAS2, or hyperactivation of Rho1 restored both the viability and the transcriptional function (both ribosomal and Msn2/Msn4-dependent gene expression) in the mtl1 mutant to almost wild type levels when cells were starved of glucose or stressed with H(2)O(2). Taking our results together, we propose an essential role for Mtl1 in signaling oxidative stress and quiescence to the CWI pathway and to the general stress response through Rho1 and the inhibition of either the TOR1 or RAS2 functions. These mechanisms would be required to allow cells to adapt to both oxidative and nutritional stresses.

Indexed as

Gene Expression Regulation, FungalOxidative StressSignal TransductionCell WallDNAFungal ProteinsGlucoseMAP Kinase Signaling SystemModels, BiologicalOligonucleotide Array Sequence AnalysisPhosphatidylinositol 3-Kinasesras ProteinsReceptors, Cell Surfacerho GTP-Binding ProteinsSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsDNAFungal ProteinsGlucoseMtl-1 protein, Cryptococcus neoformansMtl1 protein, S cerevisiaePhosphatidylinositol 3-KinasesRAS2 protein, S cerevisiaeras ProteinsReceptors, Cell SurfaceRHO1 protein, S cerevisiaerho GTP-Binding ProteinsSaccharomyces cerevisiae ProteinsTOR1 protein, S cerevisiaeTranscription Factors

Identifiers

PMID20388713
PMCPMC2885231
OpenAlexW2048143906

What OpenQuestion holds

Textmetadata
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.