ArticleMolecular genetics and genomics : MGG2014
Ecl1 is activated by the transcription factor Atf1 in response to H2O2 stress in Schizosaccharomyces pombe.
Article in Molecular genetics and genomics : MGG, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Article
- The ecl family gene ecl3+ is induced by phosphate starvation and contributes to sexual differentiation in fission yeast.Journal of cell science · 2023Article
- Sporulation: A response to starvation in the fission yeast Schizosaccharomyces pombe.MicrobiologyOpen · 2022Review
- Response to leucine in Schizosaccharomyces pombe (fission yeast).FEMS yeast research · 2022Review
- A novel cascade allows Metarhizium robertsii to distinguish cuticle and hemocoel microenvironments during infection of insects.PLoS biology · 2021Article
- Response to sulfur in Schizosaccharomyces pombe.FEMS yeast research · 2021Article
- Extension of chronological lifespan in Schizosaccharomyces pombe.Genes to cells : devoted to molecular & cellular mechanisms · 2021Review
- Genes affecting the extension of chronological lifespan in Schizosaccharomyces pombe (fission yeast).Molecular microbiology · 2021Review
- Leucine depletion extends the lifespans of leucine-auxotrophic fission yeast by inducing Ecl1 family genes via the transcription factor Fil1.Molecular genetics and genomics : MGG · 2019Article
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Authors and funding
5 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The Ecl1 family genes extend the lifespan of fission yeast when overexpressed. They also cause resistance against H(2)O(2) stress. In this study, we found that the bZip transcription factor Atf1 is a direct activator of the induction of extender of chronological lifespan (ecl1 (+)) by H(2)O(2) stress. Based on ChIP analysis, we identified that Atf1 binds to the upstream DNA region of ecl1(+). Previously, we reported that overexpression of ecl1(+) increased the expression of the catalase-encoding ctt1(+). This ecl1(+)-dependent increase of ctt1(+) expression occurred in ∆atf1 mutant. On the other hand, the activation of ctt1 (+) caused by the ∆pyp1 mutation, which enhances Sty1-Atf1 activity, could occur in ∆ecl1 mutant. Based on these results, we propose that Atf1 can regulate ctt1(+) in both an Ecl1-dependent and an Ecl1-independent manner.
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