ArticleCurrent genetics2010
Overexpression of SNG1 causes 6-azauracil resistance in Saccharomyces cerevisiae.
Article in Current genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
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- A High-Copy Suppressor Screen Reveals a Broad Role of Prefoldin-like Bud27 in the TOR Signaling Pathway inGenes · 2022Article
- Rational and evolutionary engineering of Saccharomyces cerevisiae for production of dicarboxylic acids from lignocellulosic biomass and exploring genetic mechanisms of the yeast tolerance to the biomass hydrolysate.Biotechnology for biofuels and bioproducts · 2022Article
- The Association of Rpb4 with RNA Polymerase II Depends on CTD Ser5P Phosphatase Rtr1 and Influences mRNA Decay inInternational journal of molecular sciences · 2022Article
- Rpb4 and Puf3 imprint and post-transcriptionally control the stability of a common set of mRNAs in yeast.RNA biology · 2021Article
- Genetic variation in aneuploidy prevalence and tolerance across Saccharomyces cerevisiae lineages.Genetics · 2021Article
- Role of MCC/Eisosome in Fungal Lipid Homeostasis.Biomolecules · 2019Review
- Genome-Wide Signatures of Selection inFrontiers in microbiology · 2019Article
- The yeast prefoldin-like URI-orthologue Bud27 associates with the RSC nucleosome remodeler and modulates transcription.Nucleic acids research · 2014Article
- Correct assembly of RNA polymerase II depends on the foot domain and is required for multiple steps of transcription in Saccharomyces cerevisiae.Molecular and cellular biology · 2013Article
- Genome-wide H4 K16 acetylation by SAS-I is deposited independently of transcription and histone exchange.Nucleic acids research · 2012Article
- The conserved foot domain of RNA pol II associates with proteins involved in transcriptional initiation and/or early elongation.Genetics · 2011Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanism of action of 6AU, a growth inhibitor for many microorganisms causing depletion of intracellular nucleotide pools of GTP and UTP, is not well understood. To gain insight into the mechanisms leading to 6AU resistance, and in an attempt to uncover novel genes required for this resistance, we undertook a high-copy-number suppressor screening to identify genes whose overexpression could repair the 6AU(S) growth defect caused by rpb1 mutations in Saccharomyces cerevisiae. We have identified SNG1 as a multicopy suppressor of the 6AU(S) growth defect caused by the S. cerevisiae rpb1 mutant. The mechanism by which Sng1 causes 6AU resistance is independent of the transcriptional elongation and of the nucleotide-pool regulation through Imd2 and Ura2, as well as of the Ssm1-mediated 6AU detoxification. This resistance to 6AU is not extended to other uracil analogues, such as 5-fluorouracil, 5FU. In addition, our results suggest that 6AU enters S. cerevisiae cells through the uracil permease Fur4. Our results demonstrate that Sng1 is localised in the plasma membrane and evidence SNG1 and FUR4 genes as determinants of resistance and susceptibility to this inhibitory compound, respectively. Taken together, these results show new mechanisms involved in the resistance and susceptibility to 6AU.
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