ArticleCurrent genetics2008
Oxidant resistance in a yeast mutant deficient in the Sit4 phosphatase.
Article in Current genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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
5 citing papers in PubMed, 8 citations in OpenAlex.
- Experimental evolution of Saccharomyces cerevisiae for caffeine tolerance alters multidrug resistance and target of rapamycin signaling pathways.G3 (Bethesda, Md.) · 2024Article
- Experimental evolution ofbioRxiv : the preprint server for biology · 2024Article
- The ceramide-activated protein phosphatase Sit4p controls lifespan, mitochondrial function and cell cycle progression by regulating hexokinase 2 phosphorylation.Cell cycle (Georgetown, Tex.) · 2016Article
- The core regulation module of stress-responsive regulatory networks in yeast.Nucleic acids research · 2012Article
- Role for Sit4p-dependent mitochondrial dysfunction in mediating the shortened chronological lifespan and oxidative stress sensitivity of Isc1p-deficient cells.Molecular microbiology · 2011Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Resistance to thiol oxidation can arise from mutations altering redox homeostasis. A Saccharomyces cerevisiae sit4-110 mutant is here described, which was isolated as resistant to the thiol-specific oxidant dipyridyl disulfide (DPS) and which contains a single-residue substitution in the SIT4 gene. Sit4p is a protein phosphatase with multiple roles in signal transduction through the target-of-rapamycin (TOR) pathway. We found that sit4-110 elevates the levels of glutathione. However, this cannot be the (only) cause for the DPS-resistance, since sit4-110 also conferred DPS/H2O2-resistance in a glutathione-deficient strain. Of the known Sit4p substrates, only Tip41p is involved in DPS-resistance; both Delta tip41 deletion and overexpression of the Tip41p target Tap42p resulted in increased DPS-resistance. Thus, the role of Sit4p in DPS-tolerance differs from its role during TOR-inactivation and salt stress. In view of Tap42p's known involvement in actin homeostasis, sit4-110 could compensate for putative actin-related defects caused by DPS. However, sit4-110 has pronounced actin polarization defects under both absence and presence of DPS. A relation between actin homeostasis and DPS resistance of sit4-110 cannot be ruled out, but our results suggest that unknown pathways might be involved in DPS resistance through mechanisms involving the Sit4p and/or Tap42p function(s).
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Registered trials
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.