Sensitivity to Lovastatin of Saccharomyces cerevisiae Strains Deleted for Pleiotropic Drug Resistance (PDR) Genes

2011 ◽  
Vol 20 (4) ◽  
pp. 191-195 ◽  
Author(s):  
Luca Riccardo Formenti ◽  
Morten C. Kielland-Brandt
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Drug Resistance ◽  
Pleiotropic Drug Resistance

Pleiotropic drug-resistance attenuated genomic library improves elucidation of drug mechanisms

2015 ◽  
Vol 11 (11) ◽  
pp. 3129-3136 ◽  
Author(s):  
Namal V. C. Coorey ◽  
James H. Matthews ◽  
David S. Bellows ◽  
Paul H. Atkinson
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Drug Resistance ◽  
Mechanism Of Action ◽  
Gene Deletion ◽  
Genomic Library ◽  
Deletion Mutants ◽  
Pleiotropic Drug Resistance ◽  
Genome Wide

Identifying Saccharomyces cerevisiae genome-wide gene deletion mutants that confer hypersensitivity to a xenobiotic aids the elucidation of its mechanism of action (MoA).

Heterologous carotenoid production in Saccharomyces cerevisiae induces the pleiotropic drug resistance stress response

Yeast ◽  
2010 ◽  
Vol 27 (12) ◽  
pp. 983-998 ◽  
Author(s):  
René Verwaal ◽  
Yang Jiang ◽  
Jing Wang ◽  
Jean-Marc Daran ◽  
Gerhard Sandmann ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Drug Resistance ◽  
Stress Response ◽  
Pleiotropic Drug Resistance ◽  
Carotenoid Production

scholarly journals RPD3 and UME6 are involved in the activation of PDR5 transcription and pleiotropic drug resistance in ρ0 cells of Saccharomyces cerevisiae

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yoichi Yamada
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Drug Resistance ◽  
Positive Response ◽  
Mrna Levels ◽  
Transporter Gene ◽  
Transcriptional Expression ◽  
Pleiotropic Drug Resistance ◽  
Wild Type ◽  
Binding Partners ◽  
Retrograde Signalling

Abstract Background In Saccharomyces cerevisiae, the retrograde signalling pathway is activated in ρ0/− cells, which lack mitochondrial DNA. Within this pathway, the activation of the transcription factor Pdr3 induces transcription of the ATP-binding cassette (ABC) transporter gene, PDR5, and causes pleiotropic drug resistance (PDR). Although a histone deacetylase, Rpd3, is also required for cycloheximide resistance in ρ0/− cells, it is currently unknown whether Rpd3 and its DNA binding partners, Ume6 and Ash1, are involved in the activation of PDR5 transcription and PDR in ρ0/− cells. This study investigated the roles of RPD3, UME6, and ASH1 in the activation of PDR5 transcription and PDR by retrograde signalling in ρ0 cells. Results ρ0 cells in the rpd3∆ and ume6∆ strains, with the exception of the ash1∆ strain, were sensitive to fluconazole and cycloheximide. The PDR5 mRNA levels in ρ0 cells of the rpd3∆ and ume6∆ strains were significantly reduced compared to the wild-type and ash1∆ strain. Transcriptional expression of PDR5 was reduced in cycloheximide-exposed and unexposed ρ0 cells of the ume6∆ strain; the transcriptional positive response of PDR5 to cycloheximide exposure was also impaired in this strain. Conclusions RPD3 and UME6 are responsible for enhanced PDR5 mRNA levels and PDR by retrograde signalling in ρ0 cells of S. cerevisiae.

scholarly journals Involvement of the Pleiotropic Drug Resistance Response, Protein Kinase C Signaling, and Altered Zinc Homeostasis in Resistance of Saccharomyces cerevisiae to Diclofenac

2011 ◽  
Vol 77 (17) ◽  
pp. 5973-5980 ◽  
Author(s):  
Jolanda S. van Leeuwen ◽  
Nico P. E. Vermeulen ◽  
J. Chris Vos
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Drug Resistance ◽  
Cell Wall ◽  
Transcription Factor ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Zinc Homeostasis ◽  
Yeast Cells ◽  
Pleiotropic Drug Resistance ◽  
Kinase C

ABSTRACTDiclofenac is a widely used analgesic drug that can cause serious adverse drug reactions. We usedSaccharomyces cerevisiaeas a model eukaryote with which to elucidate the molecular mechanisms of diclofenac toxicity and resistance. Although most yeast cells died during the initial diclofenac treatment, some survived and started growing again. Microarray analysis of the adapted cells identified three major processes involved in diclofenac detoxification and tolerance. In particular, pleiotropic drug resistance (PDR) genes and genes under the control of Rlm1p, a transcription factor in the protein kinase C (PKC) pathway, were upregulated in diclofenac-adapted cells. We tested if these processes or pathways were directly involved in diclofenac toxicity or resistance. Of the pleiotropic drug resistance gene products, the multidrug transporter Pdr5p was crucially important for diclofenac tolerance. Furthermore, deletion of components of the cell wall stress-responsive PKC pathway increased diclofenac toxicity, whereas incubation of cells with the cell wall stressor calcofluor white before the addition of diclofenac decreased its toxicity. Also, diclofenac induced flocculation, which might trigger the cell wall alterations. Genes involved in ribosome biogenesis and rRNA processing were downregulated, as were zinc-responsive genes. Paradoxically, deletion of the zinc-responsive transcription factor Zap1p or addition of the zinc chelator 1,10-phenanthroline significantly increased diclofenac toxicity, establishing a regulatory role for zinc in diclofenac resistance. In conclusion, we have identified three new pathways involved in diclofenac tolerance in yeast, namely, Pdr5p as the main contributor to the PDR response, cell wall signaling via the PKC pathway, and zinc homeostasis, regulated by Zap1p.

Upregulated pleiotropic drug resistance genes in Saccharomyces cerevisiae yrr1–52

The Nucleus ◽  
2015 ◽  
Vol 58 (3) ◽  
pp. 231-234
Author(s):  
Naohiko Kodo ◽  
Shoei Sakata ◽  
Toshiro Matsuda
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Drug Resistance ◽  
Resistance Genes ◽  
Pleiotropic Drug Resistance
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