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  • 1
    Electronic Resource
    Electronic Resource
    Genotoxicity of river water under the influence of petrochemical industrial complexes (1994)
    Springer
    Bulletin of environmental contamination and toxicology 52 (1994), S. 848-855 
    Details
    ISSN: 1432-0800
    Source: Springer Online Journal Archives 1860-2000
    Topics: Energy, Environment Protection, Nuclear Power Engineering , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00200693
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  • 2
    Electronic Resource
    Electronic Resource
    Reassessing the genotoxic potential of 8-MOP + UVA-induced DNA damage in the yeast Saccharomyces cerevisiae (1989)
    Springer
    Current genetics 16 (1989), S. 75-80 
    Details
    ISSN: 1432-0983
    Keywords: Saccharomyces cerevisiae ; Psoralen photoaddition ; Interstrand cross-link ; Repair deficiency ; Genotoxicity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Two different UVA irradiation systems were initially biologically calibrated with two haploid yeast strains proficient and deficient, respectively, in nucleotide excision repair. The number of DNA lesions introduced into the cell's genome by the photoactivated bifunctional furocoumarin 8-MOP was then calculated by means of the applied UVA exposure doses. At LD37 the repair-proficient wild type had about 14 ICL and 34 furan-side monoadducts in its DNA, while doubly blocked repair mutant rad3-12 pso1-1 had 2 ICL and 3 monoadducts. Locus-specific reversion of lys1-1 followed two-hit kinetics in the repair-proficient wild type and one-hit kinetics in an excision-deficient rad2-20 mutant, as would be expected if ICL was the main type of mutagenic lesion in the wild type and monoadducts the main mutagenic lesion type in the excision-deficient strain. Quantitative comparison of 8-MOP + UVA-induced ICL with those induced by bifunctional mustard revealed the former to have a much higher genotoxicity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00393398
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  • 3
    Electronic Resource
    Electronic Resource
    Genetic effects of photoactivated psoralens during meiosis in DNA repair mutantpso3-1 ofSaccharomyces cerevisiae (1994)
    Springer
    Current genetics 25 (1994), S. 19-23 
    Details
    ISSN: 1432-0983
    Keywords: Psoralen ; DNA repair mutants ; Gene conversion ; Recombination ; Saccharomyces cerevisiae
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The influence of the DNA repair genePSO3 on photoactivated psoralen-induced meiotic recombination, gene conversion, reverse mutation, and on survival, was assayed in diploid strains ofSaccharomyces cerevisiae homozygous for the wild-type or thepso3-1 mutant allele. Sporulation was normal in thepso3-1 diploid. Wild-type and mutant strains had the same sensitivity to photoactivated monofunctional psoralen (3-CPs+UVA) in meiosis-uncommitted and meiosis-committed stages. The mutant showed higher sensitivity to photoactivated bifunctional psoralen (8-MOP+UVA) during all stages of the meiotic cycle. Mutation induction by 3-CPs+UVA or 8-MOP+UVA in meiosis-committed cells revealed no significant differences between wild-type and thepso3-1 mutant. The status of thePSO3 gene has no influence on the kinetics of induction of gene conversion and crossing-over after 3-CPs+UVA treatment in meiosis-committed cells: gene conversion was blocked while recombination was induced. After treatment with 8-MOP+UVA gene conversion was also blocked in both strains while crossing-over could only be observed in meiosis-committed wild-type cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00712961
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  • 4
    Electronic Resource
    Electronic Resource
    Low glutathione pools in the original pso3 mutant of Saccharomyces cerevisiae are responsible for its pleiotropic sensitivity phenotype (1998)
    Springer
    Current genetics 33 (1998), S. 4-9 
    Details
    ISSN: 1432-0983
    Keywords: Key words Petite mutation ; Error-prone repair ; Paraquat ; Psoralen photo-induced DNA-damage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The original pso3-1 mutant isolate of the yeast Saccharomyces cerevisiae exhibits a pleiotropic mutagen-sensitivity phenotype that includes sensitivity to UVA-activated 3-carbethoxypsoralen, to UVC-light, to mono- and bi-functional nitrogen mustard, to paraquat, and to cadmium; on the other hand, it shows hyper-resistance (HYR) to nitrosoguanidine when compared to established wild-type strains. Also, the original pso3-1 mutant exhibits a low UVC-induced mutability and mitotic gene conversion and a high rate of spontaneous and UVC-induced petite mutations. Since the HYR to the nitrosoguanidine (MNNG) phenotype resembles that of low glutathione-containing yeast cells, the original pso3-1 mutant was crossed to a gsh1 knock-out mutant that lacks the enzyme for the first step in glutathione biosynthesis and the resulting diploid was tested for complementation. While there was none for HYR to nitrosoguanidine, and other low glutathione-related phenotypes, some other phenotypic characteristics of pso3-1, e.g. UVC sensitivity and UVC-induced mutability were restored to a wild-type level. Tetrad analysis of a diploid derived from a cross of the original haploid pso3-1 isolate with a repair-proficient, normal glutathione-containing, PSO3 GSH1 wild-type led to the separation of a leaky gsh1 mutation phenotype from that of the repair-deficient pso3-1 phenotype. Linkage studies by tetrad and random spore analyses indicated no linkage of the two genes. This shows that the low glutathione content in the original pso3-1 isolate is due to a second, additional, mutation in the GSH1 locus and is unrelated to the pso3-1 mutation. Thus, the original pso3-1 isolate is a pso3-1 gsh1 double mutant with most of the particular characteristics of the pleiotropic sensitivity phenotype contributed by either the pso3-1 or the gsh1-leaky mutant allele. The expression of a few phenotypic characteristics of pso3, however, were most pronounced in pso3-1 mutants with a low glutathione pool.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002940050301
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  • 5
    Electronic Resource
    Electronic Resource
    Isolation and characterization of three mutants with increased sensitivity to photoactivated 3-carbethoxypsoralen in Saccharomyces cerevisiae (1994)
    Springer
    Current genetics 25 (1994), S. 407-411 
    Details
    ISSN: 1432-0983
    Keywords: Psoralen sensitivity ; Saccharomyces cerevisiae ; DNA repair ; Oxidative stress
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The complementation and genetical analysis of yeast mutants sensitive to photoactivated 3-carbethoxy-psoralen define three novel recessive mutant alleles pso-5-1, pso6-1, and pso7-1. Their cross-sensitivity to UV254nm, radiomimetic mutagens, and to chemicals enhancing oxidative stress suggest that these mutants are either impaired in metabolic steps protecting from oxidative stress or in mechanisms of the repair of oxygen-dependent DNA lesions. None of the three novel mutant alleles block the induction of reverse mutation by photoactivated mono- and bi-functional psoralens, nitrogen mustards, or UV254nm.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00351778
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  • 6
    Electronic Resource
    Electronic Resource
    The Saccharomyces cerevisiae gene PSO5/RAD16 is involved in the regulation of DNA damage-inducible genes RNR2 and RNR3 (1998)
    Springer
    Current genetics 34 (1998), S. 124-127 
    Details
    ISSN: 1432-0983
    Keywords: Key wordsPSO5/RAD16 ; Saccharomyces cerevisiae ; Nucleotide excision repair ; Oxidative stress ; Ribonucleotide reductase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The expression of β-galactosidase from DNA damage-inducible RNR2-lacZ and RNR3-lacZ fusion constructs was compared in wild-type (WT) and pso5/rad16 mutant strains after treatment with five mutagens/oxidative stressors. While exposure to the mutagens UVC, 4NQO and H2O2 induced expression of the RNR2-lacZ and RNR3-lacZ fusion constructs in two WT strains, treatment with the two oxidative stressors tBOOH and paraquat did not. In the pso5-1 mutant induction of RNR2-lacZ was largely reduced after UVC and H2O2 while there was no significant induction of β-galactosidase expression after 4NQO treatment for this construct. For RNR3-lacZ there was strongly reduced expression of pso5-1 after UVC and 4NQO while H2O2 failed to induce expression of β-galactosidase. In the WT strains the ranking of the inducing power of the mutagens at 90% survival (as measured in the pso5-1 mutant) was 4NQO〉UVC〉H2O2. Though the WT strains were clearly more resistant that the pso5-1 mutant to the two oxidative stressors paraquat and tBOOH, these substances failed to significantly enhance expression of the RNR2-lacZ and RNR3-lacZ fusion constructs in both the WT and the pso5-1 mutant. Our data suggest that Pso5p/Rad16p has a function in the signal transducing pathway controlling DNA damage-inducible components of nucleotide excision repair.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002940050376
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  • 7
    Electronic Resource
    Electronic Resource
    Gene PSO5 of Saccharomyces cerevisiae, involved in repair of oxidative DNA damage, is allelic to RAD16 (1995)
    Springer
    Current genetics 27 (1995), S. 493-495 
    Details
    ISSN: 1432-0983
    Keywords: DNA ; Repair ; Psoralen photoaddition ; Yeast mutant ; Oxidative DNA damage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The pos5-1 mutation renders Saccharomyces cerevisiae cells sensitive to DNA-damaging agents. We have isolated plasmids from a S. cerevisiae genomic library capable of restoring wild-type levels of 254-nm ultraviolet light sensitivity of the pso5-1 mutant. DNA sequence analysis revealed that the complementing activity resides in RAD16, a gene involved in excision repair. Tetrad analysis showed that PSO5, like RAD16, is tightly linked to LYS2 on chromosome II. Moreover, allelism between the pso5-1 and rad16 mutants was demonstrated by the comparison of mutagen sensitivity phenotypes, complementation tests, and by meiotic analysis. The cloned RAD16 gene was capable of restoring wild-type resistance of the pso5-1 mutant to H2O2 and photoactivated 3-carbethoxypsoralen, both treatments generating oxidative stress-related DNA damage. This indicates that RAD16/PSO5 might also participate in the repair of oxidative base damage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00314437
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  • 8
    Electronic Resource
    Electronic Resource
    Interaction between genes controlling sensitivity to psoralen (pso) and to radiation (rad) after 3-carbethoxypsoralen plus 365 nm UV light treatment in yeast (1985)
    Springer
    Molecular genetics and genomics 201 (1985), S. 415-420 
    Details
    ISSN: 1617-4623
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Using various double mutant combinations and single mutants, the interactions between the pso1 and the pso2 mutations as well as with rad mutations blocking the excision-resynthesis, the mutagenic and the recombinogenic repair pathways were analysed in Saccharomyces cerevisiae following 3-carbethoxypsoralen (3-CPs) photoaddition. Results obtained with this monofunctional agent, which induces only 4′,5′ monoadducts in DNA following UVA (365 nm) irradiation, were compared to previous data obtained after photoaddition of the bifunctional derivative, 8-methoxypsoralen (8-MOP) which induces both monoadducts and interstrand cross links. From cell survival responses, it is clear that the repair of these two types of lesion share common steps. However non-epistatic interactions are observed between pso1 and pso2, pso1 and Rad52 (blocked in the recombinogenic pathway), and rad3 (blocked in the excision pathway) and rad52 after 3-CPs photoaddition, whereas epistatic interactions between these mutants were found after 8-MOP photoaddition. From this it can be concluded that for specific repair steps monoadducts are likely to be recognized as substrates distinct from cross links.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00331332
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  • 9
    Electronic Resource
    Electronic Resource
    The pso4-1 mutation reduces spontaneous mitotic gene conversion and reciprocal recombination in Saccharomyces cerevisiae (1992)
    Springer
    Molecular genetics and genomics 235 (1992), S. 311-316 
    Details
    ISSN: 1617-4623
    Keywords: pso4-1 mutation ; Saccharomyces cerevisiae ; Mitotic recombination ; 8-Methoxypsoralen photoreaction ; his4 gene duplication
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Spontaneous mitotic recombination was examined in the haploid pso4-1 mutant of Saccharomyces cerevisiae and in the corresponding wild-type strain. Using a genetic system involving a duplication of the his4 gene it was shown that the pso4-1 mutation decreases at least fourfold the spontaneous rate of mitotic recombination. The frequency of spontaneous recombination was reduced tenfold in pso4-1 strains, as previously observed in the rad52-1 mutant. However, whereas the rad52-1 mutation specifically reduces gene conversion, the pso4-1 mutation reduces both gene conversion and reciprocal recombination. Induced mitotic recombination was also studied in pso4-1 mutant and wild-type strains after treatment with 8-methoxypsoralen plus UVA and 254 nm UV irradiation. Consistent with previous results, the pso4-1 mutation was found strongly to affect recombination induction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00279375
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  • 10
    Electronic Resource
    Electronic Resource
    Lethality and “petite” mutation induced by the photoaddition of 8-methoxypsoralen in yeast (1977)
    Springer
    Molecular genetics and genomics 158 (1977), S. 63-72 
    Details
    ISSN: 1617-4623
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary The induction of lethal events and cytoplasmic “petite” mutations in random and synchronously dividing cultures of haploid and diploid cells of Saccharomyces cerevisiae was determined after treatment with 8-Methoxypsoralen plus 365 nm light. Diploid cells were always more resistant than haploid cells in stationary phase whereas in exponential phase haploid and diploid cells demonstrated the same response. For both degrees of ploidy exponential phase cells were more resistant than stationary phase. Mitotic recombination is induced with the same efficiency in both phases. Dark holding reduces the frequency of recombinants. In diploid cells the recovery of survival after dark holding was more pronounced than in haploid cells. The “petite” mutation is induced more efficiently in stationary phase cells than in exponential phase cells. The ρ− frequency observed on dark holding depends upon the growth phases and ploidy. As after UV irradiation in a synchronized population, G1 cells were the most sensitive as compared to S and G2 phase cells after 8-Methoxypsoralen plus light treatment. The most sensitive stages are the ones which show the highest recovery after dark holding. The cyclic pattern of ρ− induction does not appear to be strictly correlated with that of the lethal effect. In S-G2 phase cells the ρ− frequency decreased after delayed plating. The results are interpreted assuming that the excision repair acts mainly in the G1 phase whereas an efficient recombinational type of repair operates in G2. The diploid condition appears to favour this last process.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00455120
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