Common Repair Pathways Acting Upon U.V.- and X-ray Induced Damage in Diploid Cells of<i>Saccharomyces Cerevisiae</i>

Nunes, Elia; Brum, Graciela S.; Candreva, Ema C.; Frascino, Ana Clara Schenberg

doi:10.1080/09553008414550861

Cited by 13 publications

(10 citation statements)

References 30 publications

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“…In this context, the RAD24 gene is involved in excision as well as in recombination repair of UV and X-ray damage (7). XS genes (XS6, XS8, and XS9 = PS04) are also involved in both types of repair (13,30). Although differential repair is the most likely explanation for the results, it is not the only one possible.…”

Section: Discussionmentioning

confidence: 87%

“…Since suppression of the rad6-1 mutant is frequently observed (20,37), UV sensitivity was tested as described by Nunes et al (30). We obtained the expected sensitivity for a nonsuppressed rad6-1 strain (20).…”

Section: Methodsmentioning

confidence: 99%

“…The liquid medium YED contained 0.5% yeast extract (Difco) and 1% dextrose (Difco). Cells were plated on YED medium (YEDA) solidified by 2% agar (Difco) (30).…”

Section: Methodsmentioning

confidence: 99%

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Effects of bleomycin on growth kinetics and survival of Saccharomyces cerevisiae: a model of repair pathways

1992

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In order to analyze the roles of some repair genes in the processing of bleomycin-induced DNA damage and, especially, the interrelationships among the involved repair pathways, we investigated the potentially lethal effect of bleomycin on radiosensitive mutants of Saccharomyces cerevisiae defective in recombination, excision, and R4D6-dependent DNA repair. Using single, double, and triple rad mutants, we analyzed growth kinetics and survival curves as a function of bleomycin concentration. Our results indicate that genes belonging to the three epistasis groups interact in the repair of bleomycin-induced DNA damage to different degrees depending on the concentration of bleomycin. The most important mechanisms involved are recombination and postreplication repair. The initial action of a potentially inducible excision repair gene could provide intermediate substrates for the R4D6-and RAD52-dependent repair processes. Interaction between R4D6 and RADS2 genes was epistatic for low bleomycin concentrations. RA1D3 and RAD52 genes act independently in processing DNA damage induced by high concentrations of bleomycin. The synergistic interaction observed at high concentrations in the triple mutant rad2-6 rad6-1 rad52-1 indicates partial independence of the involved repair pathways, with possible common substrates. On the basis of the present results, we propose a heuristic model of bleomycin-induced DNA damage repair.Bleomycin (BLM) is a radiomimetic glycopeptide antibiotic used extensively in tumor therapy (32,48). This drug binds to DNA and through a free-radical-based mechanism produces DNA base loss and single-and double-strand breaks (43,44). In different lines of eukaryotic cells, BLM produces inhibition of DNA synthesis (10) as well as cell cycle G2 delay (19,38). With phages, bacteria, and yeast cells, it was demonstrated that this drug is recombinogenic and mutagenic (11,23,39,42). Analysis of BLM-induced mutagenesis in repackaged lambda phage suggests SOS repair dependence (33).BLM-induced DNA damage in prokaryotic and eukaryotic cells is partially reparable (3,22,27,40). For human fibroblasts, a long-patch mode of excision repair of BLM-induced damage was recently described (4, 5). Using haploid and diploid radiosensitive strains of Saccharomyces cerevisiae, Moore (22) showed that all rad single mutants sensitive to BLM tested, with the exception of rad1S, are sensitive to X rays. Likewise, BLM-sensitive (blm) mutants exhibit crosssensitivity to ionizing radiation and hydrogen peroxide (26). These results suggest that some aspects of the repair of BLM and ionizing radiation DNA damage in yeast cells may be similar. Furthermore, DNA ligase (the product of the CDC9 gene) is required in the overall process of restoring full-size DNA molecules from DNA fragments produced by BLM (24, 25).We have recently shown that BLM induces at least one error-prone type of repair in S. cerevisiae and that the PS04 (XS9) gene acts as a mutation-triggering factor (39). Furthermore, the combination of UV light and BLM produces di...

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Section: Discussionmentioning

confidence: 87%

Section: Methodsmentioning

confidence: 99%

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Effects of bleomycin on growth kinetics and survival of Saccharomyces cerevisiae: a model of repair pathways

1992

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“…1, panel C; Table 1). In fact, in the haploid state this mutation confers sensitivity only to cells in logarithmic phase of growth (Nunes et al 1984;Henriques et al 1989). Figure 1, panels D and E shows that the pso4-1 diploid cells are more sensitive than the wild-type diploid cells to the lethal effect of mono-(HN1) and bifunctional (HN2) alkylating agents in both growth phases.…”

Section: Survival After Treatment With 254 Nm Uv Radiationmentioning

confidence: 97%

ThePSO4 gene is responsible for an error-prone recombinational DNA repair pathway inSaccharomyces cerevisiae

et al. 1989

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The induction of mitotic gene conversion and crossing-over in Saccharomyces cerevisiae diploid cells homozygous for the pso4-1 mutation was examined in comparison to the corresponding wild-type strain. The pso4-1 mutant strain was found to be completely blocked in mitotic recombination induced by photoaddition of mono- and bifunctional psoralen derivatives as well as by mono- (HN1) and bifunctional (HN2) nitrogen mustards or 254 nm UV radiation in both stationary and exponential phases of growth. Concerning the lethal effect, diploids homozygous for the pso4-1 mutation are more sensitive to all agents tested in any growth phase. However, this effect is more pronounced in the G2 phase of the cell cycle. These results imply that the ploidy effect and the resistance of budding cells are under the control of the PSO4 gene. On the other hand, the pso4-1 mutant is mutationally defective for all agents used. Therefore, the pso4-1 mutant has a generalized block in both recombination and mutation ability. This indicates that the PSO4 gene is involved in an error-prone repair pathway which relies on a recombinational mechanism, strongly suggesting an analogy between the pso4-1 mutation and the RecA or LexA mutation of Escherichia coli.

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“…We used the haploid strain of Saccharomyces cerevisiae SC7K(lys2-3), auxotrophic mutation affecting the coding of Lysine in the locus 2-3 (Nunes et al 1984), derived from SC7K (Saccharomyces cerevisiae #7K, wild type strain) (Benathen and Beam 1977). …”

Section: Yeast Strainmentioning

confidence: 99%

Lethal and mutagenic interactions between γ-rays, cisplatin and etoposide at the cellular and molecular levels

Lillo

Bracesco

Nunes

2010

International Journal of Radiation Biology

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Common Repair Pathways Acting Upon U.V.- and X-ray Induced Damage in Diploid Cells ofSaccharomyces Cerevisiae

Cited by 13 publications

References 30 publications

Effects of bleomycin on growth kinetics and survival of Saccharomyces cerevisiae: a model of repair pathways

Effects of bleomycin on growth kinetics and survival of Saccharomyces cerevisiae: a model of repair pathways

ThePSO4 gene is responsible for an error-prone recombinational DNA repair pathway inSaccharomyces cerevisiae

Lethal and mutagenic interactions between γ-rays, cisplatin and etoposide at the cellular and molecular levels

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