Evidence map›Paper›PMID 25487302›Full record

ArticleCurrent genetics2015

Activation of the mitochondrial signaling pathway in response to organic solvent stress in yeast.

Nao Nishida-Aoki, Hitoshi Mori, Kouichi Kuroda, Mitsuyoshi Ueda

Abstract read
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In one paragraph

Article in Current genetics, 2015. 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
–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

10 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Mec1Current genetics · 2018
    Article
  10. 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

4 authors.

Nao Nishida-AokiDivision of Applied Life Sciences, Graduate School of Agriculture, Kyoto University, Sakyo-ku, Kyoto, 606-8502, Japan.
Hitoshi Mori
Kouichi Kuroda
Mitsuyoshi Ueda

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In Saccharomyces cerevisiae, we have demonstrated that organic solvent stress activated the pleiotropic drug resistance (PDR) pathway, which involves the transcription factors Pdr1p and Pdr3p. Pdr1p and Pdr3p are functionally homologous in multidrug resistance, although Pdr3p has been reported to have some distinct functions. Here, we analyzed the functions of Pdr1p and Pdr3p during the cellular response to isooctane, as a representative of organic solvents, and observed the differential functions of Pdr1p and Pdr3p. In response to organic solvent stress, only Pdr3p contributed to the regulation of downstream genes of the PDR pathway, while Pdr1p had a rather inhibitory role on transcriptional induction through competition with Pdr3p for binding to their recognition sequence, pleiotropic drug response element. Our results demonstrated that organic solvent stress was likely to damage mitochondria, causing generation of reactive oxygen species and mitochondrial fragmentation, and to activate retrograde signaling pathway via Pdr3p to upregulate PDR5 expression. Therefore, the unique function of Pdr3p in organic solvent stress distinguishes this pathway from the multidrug response.

Indexed as

ATP-Binding Cassette TransportersDNA-Binding ProteinsDrug Resistance, FungalGene Expression Regulation, FungalMitochondriaOctanesReactive Oxygen SpeciesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSignal TransductionStress, PhysiologicalTranscription Factors2,2,4-trimethylpentaneATP-Binding Cassette TransportersDNA-Binding ProteinsOctanesPDR1 protein, S cerevisiaePDR3 protein, S cerevisiaePDR5 protein, S cerevisiaeReactive Oxygen SpeciesSaccharomyces cerevisiae ProteinsTranscription Factors

Identifiers

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Registered trials

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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.