ArticleGenetics1998
The transcriptional activator Imp2p maintains ion homeostasis in Saccharomyces cerevisiae.
Article in Genetics, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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Who cites it
6 citing papers in PubMed, 16 citations in OpenAlex.
- The prefoldin complex regulates chromatin dynamics during transcription elongation.PLoS genetics · 2013Article
- Functional identification of Arabidopsis stress regulatory genes using the controlled cDNA overexpression system.Plant physiology · 2008Article
- Isolation and characterization of Saccharomyces cerevisiae mutants with enhanced resistance to the anticancer drug bleomycin.Current genetics · 2004Article
- Protective mechanisms against the antitumor agent bleomycin: lessons from Saccharomyces cerevisiae.Current genetics · 2003Review
- Disruption of the Saccharomyces cerevisiae cell-wall pathway gene SLG1 causes hypersensitivity to the antitumor drug bleomycin.Molecular genetics and genomics : MGG · 2003Article
- Pir1p mediates translocation of the yeast Apn1p endonuclease into the mitochondria to maintain genomic stability.Molecular and cellular biology · 2001Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Yeast cells deficient in the transcriptional activator Imp2p are viable, but display marked hypersensitivity to a variety of oxidative agents. We now report that imp2 null mutants are also extremely sensitive to elevated levels of the monovalent ions, Na+ and Li+, as well as to the divalent ions Ca2+, Mn2+, Zn2+, and Cu2+, but not to Cd2+, Mg2+, Co2+, Ni2+, and Fe2+, as compared to the parent strain. We next searched for multicopy suppressor genes that would allow the imp2Delta mutant to grow under high salt conditions. Two genes that independently restored normal salt-resistance to the imp2Delta mutant, ENA1 and HAL3, were isolated. ENA1 encodes a P-type ion pump involved in monovalent ion efflux from the cell, while HAL3 encodes a protein required for activating the expression of Ena1p. Neither ENA1 nor HAL3 gene expression was positively regulated by Imp2p. Moreover, the imp2 ena1 double mutant was exquisitely sensitive to Na+/Li+ cations, as compared to either single mutant, implying that Imp2p mediates Na+/Li+ cation homeostasis independently of Ena1p.
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