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  • 1
    Electronic Resource
    Electronic Resource
    Mutant allele pso7-1, that sensitizes Saccharomyces cerevisiae to photoactivated psoralen, is allelic with COX11, encoding a protein indispensable for a functional cytochrome c oxidase (1999)
    Springer
    Current genetics 36 (1999), S. 124-129 
    Details
    ISSN: 1432-0983
    Keywords: Key words Psoralen sensitivity ; Cytochrome oxidase ; Saccharomyces cerevisiae ; Oxidative stress
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The yeast gene PSO7 was cloned from a genomic library by complementation of the pso7-1 mutant's sensitivity phenotype to 4-nitroquinoline-1-oxide (4NQO). Sequence analysis revealed that PSO7 is allelic to the 1.1-kb ORF of the yeast gene COX11 which is located on chromosome XVI and encodes a protein of 28-kDa localized in the inner mitochondrial membrane. Allelism of PSO7/COX11 was verified by non-complementation of 4NQO-sensitivity in diploids homo- and hetero-allelic for the pso7-1 and cox11::TRP1 mutant alleles. Sensitivity to 4NQO was the same in exponentially growing cells of the pso7-1 mutant and the cox11::TRP1 disruptant. Allelism of COX11 and PSO7 indicates that the pso7 mutant's sensitivity to photoactivated 3-carbethoxypsoralen and to 4NQO is not caused by defective DNA repair, but rather is due to an altered metabolism of the pro-mutagen 4NQO in the absence of cytochrome oxidase (Cox) in pso7-1/cox11::TRP1 mutants/disruptants. Lack of Cox might also lead to a higher reactivity of the active oxygen species produced by photoactivated 3-carbethoxypsoralen. The metabolic state of the cells is important for their sensitivity phenotype since the largest enhancement of sensitivity to 4NQO between wild-type (WT) and the pso7 mutant occurs in exponentially growing cells, while cells in stationary phase or growing cells in phosphate buffer have the same 4NQO resistance, irrespective of their WT/mutant status. Strains containing the pso7-1 or cox11::TRP1 mutant allele were also sensitive to the oxidative stress-generating agents H2O2 and paraquat. Mutant pso7-1, as well as disruptant cox11::TRP1, harboured mitochondria that in comparison to WT contained less than 5% and no detectable Cox activity, respectively.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002940050481
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  • 2
    Electronic Resource
    Electronic Resource
    Glutathione, but not transcription factor Yap1, is required for carbon source-dependent resistance to oxidative stress in Saccharomyces cerevisiae (2000)
    Springer
    Current genetics 37 (2000), S. 175-182 
    Details
    ISSN: 1432-0983
    Keywords: Key words Glutathione ; Yap1 ; H2O2 ; t-BOOH ; Glucose repression ; Oxidative stress ; Diauxic shift
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Resistance of haploid yeast to hydrogen peroxide and to tert-butylhydroperoxide strongly increases when 4% glucose is replaced by glycerol or ethanol as the carbon source of the complex medium. Using a GSH1-promoter-lacZ-fusion reporter construct we could demonstrate that GSH1 is one of the genes that are up-regulated during the shift from fermentative to oxidative metabolism. A gsh1 mutant did not exhibit respiratory growth resistance to H2O2, whereas it was only slightly impaired in acquiring resistance against t-BOOH in the same experimental conditions. An isogenic Δyap1 mutant, although more sensitive to oxidative stress than the wild-type (WT), could increase resistance to both peroxides by a similar factor as observed for the WT when shifted from 4% glucose to a non-fermentable carbon source. This indicates that in this case induction of resistance to oxidative stress is independent from Yap1 and from the Yap1-mediated stress response via the STRE motif.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002940050516
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  • 3
    Electronic Resource
    Electronic Resource
    Heat shock changes the response of the pso3 mutant of Saccharomyces cerevisiae to 8-methoxypsoralen photoaddition (1994)
    Springer
    Current genetics 26 (1994), S. 100-104 
    Details
    ISSN: 1432-0983
    Keywords: DNA repair ; Heat shock ; Hyperthermia ; Mutagenesis ; pso3-1 mutant ; Psoralen ; Yeast
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract A putative tolerance, induced by heat shock (HS), to the lethal and mutagenic effects of 8-methoxypsoralen (8-MOP) photoaddition and hyperthermia was analyzed in Saccharomyces cerevisiae using the wild-type strain N123 and the isogenic DNA repair-deficient mutant pso3-1. In wild-type cells, the HS (38°C for 1 h) did not modify either the survival or the mutation frequency observed after 8-MOP photoaddition, even though it conferred protection against the lethal effect of hyperthermia (50°C). In the pso3-1 mutant, HS induced an increase of the survival, and a decrease of the mutation frequency, after 8-MOP photoaddition and it also protected against the lethal effect of hyperthermia. The responses induced by HS were specific for 8-MOP photoaddition, since they were not observed after 254 nm ultraviolet-light damage. These results indicate that the protection conferred by HS depends of the type of lesion, and operates through the induction of different repair processes. In the pso3-1 mutant, HS could channel the repair intermediates to and error-free repair pathway.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00313795
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  • 4
    Electronic Resource
    Electronic Resource
    The DNA repair gene PSO3 of Saccharomyces cerevisiae belongs to the RAD3 epistasis group (1992)
    Springer
    Current genetics 21 (1992), S. 85-90 
    Details
    ISSN: 1432-0983
    Keywords: pso and rad mutants ; Repair ; S. cerevisiae ; 8-methoxypsoralen ; 3-carbethoxypsoralen
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary The mutant allele pso3-1 of Saccharomyces cerevisiae confers sensitivity to treatment with UV365nm (UVA) light-activated mono- and bi-functional psoralens. When pso3-1 is combined in double mutants with selected rad and pso mutant alleles and subjected to 8-MOP+UVA treatment, epistatic interaction with regard to survival is observed with pso1, pso2, and rad3. With the same treatment the combination of pso3-1 with rad6 and rad52 leads to synergistic interaction. For the monofunctional agent 3-carbethoxypsoralen (3-CPs) the analysis of double mutants yields the same results as with the bifunctional 8-methoxypsoralen (8-MOP) with the exception of the pso1-1pso3-1 double mutant. Here we find an additive interaction, i.e., the sensitivities of both parental strains are summed in the double mutant, which indicates a different substrate specificity of the repair activity encoded by the PSO1 and PSO3 genes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00318660
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  • 5
    Electronic Resource
    Electronic Resource
    The role of PSO and SNM genes in DNA repair of the yeast Saccharomyces cerevisiae (1990)
    Springer
    Current genetics 18 (1990), S. 387-393 
    Details
    ISSN: 1432-0983
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00309906
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    Paper (German National Licenses)
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