Evidence map›Paper›PMID 26063801›Full record

ArticleThe Journal of biological chemistry2015

Repression of the Low Affinity Iron Transporter Gene FET4: A NOVEL MECHANISM AGAINST CADMIUM TOXICITY ORCHESTRATED BY YAP1 VIA ROX1.

Soraia M Caetano, Regina Menezes, Catarina Amaral, Claudina Rodrigues-Pousada, Catarina Pimentel

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 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
2.7field-weighted citation impact, top 11% 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

10 citing papers in PubMed, 22 citations in OpenAlex.

  1. Fungal-Metal Interactions: A Review of Toxicity and Homeostasis.Journal of fungi (Basel, Switzerland) · 2021
    Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Metals in fungal virulence.FEMS microbiology reviews · 2018
    Review
  8. Article
  9. Article
  10. 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 2 institutions in 1 country.

Soraia M CaetanoFrom the Instituto de Tecnologia Química e Biológica António Xavier, Universidade Nova de Lisboa and.
Regina MenezesFrom the Instituto de Tecnologia Química e Biológica António Xavier, Universidade Nova de Lisboa and the Instituto de Biologia Experimental e Tecnológica, 2781-901 Oeiras, Portugal.ORCID http://orcid.org/0000-0003-0552-8480
Catarina AmaralFrom the Instituto de Tecnologia Química e Biológica António Xavier, Universidade Nova de Lisboa and.ORCID http://orcid.org/0000-0002-9442-2225
Claudina Rodrigues-PousadaFrom the Instituto de Tecnologia Química e Biológica António Xavier, Universidade Nova de Lisboa and pimentel@itqb.unl.pt claudina@itqb.unl.pt.ORCID http://orcid.org/0000-0002-5075-3639
Catarina PimentelFrom the Instituto de Tecnologia Química e Biológica António Xavier, Universidade Nova de Lisboa and pimentel@itqb.unl.pt claudina@itqb.unl.pt.ORCID http://orcid.org/0000-0002-5158-6414
Universidade Nova de Lisboa · PTInstituto de Biologia Experimental e Tecnológica · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cadmium is a well known mutagenic metal that can enter cells via nonspecific metal transporters, causing several cellular damages and eventually leading to death. In the yeast Saccharomyces cerevisiae, the transcription factor Yap1 plays a key role in the regulation of several genes involved in metal stress response. We have previously shown that Yap1 represses the expression of FET4, a gene encoding a low affinity iron transporter able to transport metals other than iron. Here, we have studied the relevance of this repression in cell tolerance to cadmium. Our results indicate that genomic deletion of Yap1 increases FET4 transcript and protein levels. In addition, the cadmium toxicity exhibited by this strain is completely reversed by co-deletion of FET4 gene. These data correlate well with the increased intracellular levels of cadmium observed in the mutant yap1. Rox1, a well known aerobic repressor of hypoxic genes, conveys the Yap1-mediated repression of FET4. We further show that, in a scenario where the activity of Yap1 or Rox1 is compromised, cells activate post-transcriptional mechanisms, involving the exoribonuclease Xrn1, to compensate the derepression of FET4. Our data thus reveal a novel protection mechanism against cadmium toxicity mediated by Yap1 that relies on the aerobic repression of FET4 and results in the impairment of cadmium uptake.

Indexed as

Biological TransportCadmiumCation Transport ProteinsCopper Transport ProteinsDNA-Binding ProteinsExoribonucleasesGene Expression Regulation, FungalIronIron-Binding ProteinsMutationRepressor ProteinsSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsStress, PhysiologicalTranscription FactorsCadmiumCation Transport ProteinsCopper Transport ProteinsDNA-Binding ProteinsExoribonucleasesFET4 protein, S cerevisiaeIronIron-Binding ProteinsRepressor ProteinsROX1 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsTranscription FactorsXRN1 protein, S cerevisiaeYAP1 protein, S cerevisiaecadmiumFet4gene regulationironmetalRox1stress responseYap1yeast metabolism

Identifiers

PMID26063801
PMCPMC4513117
OpenAlexW1508935937

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.