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  • DNA repair  (10)
  • Springer  (10)
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  • 1
    Electronic Resource
    Electronic Resource
    Characterization of the role played by the RAD59 gene of Saccharomyces cerevisiae in ectopic recombination (1999)
    Springer
    Current genetics 36 (1999), S. 13-20 
    Details
    ISSN: 1432-0983
    Keywords: Key words Gene conversion ; DNA repair ; Ty elements ; Genomic instability
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The RAD52 group of genes in the yeast Saccharomyces cerevisiae controls the repair of DNA damage by a recombinational mechanism. Despite the growing evidence for physical and biochemical interactions between the proteins of this repair group, mutations in individual genes show very different effects on various types of recombination. The RAD59 gene encodes a protein with similarity to Rad52p which plays a role in the repair of damage caused by ionizing radiation. In the present study we have examined the role played by the Rad59 protein in mitotic ectopic recombination and analyzed the genetic interactions with other members of the repair group. We found that Rad59p plays a role in ectopic gene conversion that depends on the presence of Rad52p but is independent of the function of the RecA homologue Rad51p and of the Rad57 protein. The RAD59 gene product also participates in the RAD1-dependent pathway of recombination between direct repeats. We propose that Rad59p may act in a salvage mechanism that operates when the Rad51 filament is not functional.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002940050467
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  • 2
    Electronic Resource
    Electronic Resource
    Cloning and integrative deletion of the RAD6 gene of Saccharomyces cerevisiae (1984)
    Springer
    Current genetics 8 (1984), S. 559-566 
    Details
    ISSN: 1432-0983
    Keywords: DNA repair ; Saccharomyces cerevisiae ; Cloning
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Three overlapping plasmids were isolated from a YEp24 library, which restore Rad+ functions to rad6-1 and rad6-3 mutants. Different subclones were made and shown to integrate by homologous recombination at the RAD6 site on chromosome VII, thus verifying the cloned DNA segments to be the RAD6 gene and not a suppressor. The gene resides in a 1.15 kb fragment, which restores Rad+ levels of resistance to U.V., MMS and γ-rays to both rad6-1 and rad6-3 strains. It also restores sporulation ability to rad6-1 diploids. Integrative deletion of the RAD6 gene was shown not to be completely lethal to the yeast. Our results suggest that the RAD6 gene has some cell cycle-specific function(s), probably during late S phase.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00395700
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  • 3
    Electronic Resource
    Electronic Resource
    The RAD50 gene of Saccharomyces cerevisiae is not essential for vegetative growth (1986)
    Springer
    Current genetics 10 (1986), S. 487-489 
    Details
    ISSN: 1432-0983
    Keywords: DNA repair ; Gene disruption
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary The gene RAD50 was located by the ability of subclones to restore the Rad+ phenotype following transformation of a rad50-1 mutant. Disruption of the gene was achieved by directed integration of a plasmid carrying a fragment internal to RAD50. Haploids with the disrupted gene are viable and do not differ in growth rate or plating efficiency from isogenic rad50-1 or Rad+ strains.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00419878
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  • 4
    Electronic Resource
    Electronic Resource
    Cloning and mapping of CDC40, a Saccharomyces cerevisiae gene with a role in DNA repair (1985)
    Springer
    Current genetics 9 (1985), S. 253-257 
    Details
    ISSN: 1432-0983
    Keywords: Saccharomyces cerevisiae ; CDC40 ; DNA repair ; Cloning ; Mapping
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary The cdc40 mutation has been previously shown to be a heat-sensitive cell-division-cycle mutation. At the restrictive temperature, cdc40 cells arrest at the end of DNA replication, but retain sensitivity to hydroxyurea (Kassir and Simchen 1978). The mutation has also been shown to affect commitment to meiotic recombination and its realization. Here we show that mutant cells are extremely sensitive to Methyl-Methane Sulfonate (MMS) when the treatment is carried out at restrictive temperature. Incubation at 37 °C prior to, or after MMS treatment at 23 °C, does not result in lower survival. It is concluded that the CDC40 gene product has a role in DNA repair, possibly holding together or protecting the DNA during the early stages of repair. The CDC40 gene was cloned on a 2.65 kb DNA fragment. A 2 μ plasmid carrying the gene was integrated and mapped to chromosome IV, between trp4 and ade8, by the method of marker loss. Conventional tetrad analysis has shown cdc40 to map 1.7 cM from trp4.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00419952
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  • 5
    Electronic Resource
    Electronic Resource
    Recombination between divergent sequences leads to cell death in a mismatch-repair-independent manner (2000)
    Springer
    Current genetics 38 (2000), S. 23-32 
    Details
    ISSN: 1432-0983
    Keywords: Key words Gene conversion ; Double-strand breaks ; DNA repair ; Mismatch repair
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Homologous recombination is an important DNA repair mechanism in vegetative cells. During the repair of double-strand breaks, genetic information is transferred between the interacting DNA sequences, thus creating a gene-conversion event. Gene conversion of a functional member of a gene family, which uses an inactive member (such as a pseudogene) as a template, might have deleterious consequences. It is therefore important for the cell to prevent recombination between divergent sequences. We have studied the repair of a double-strand break by recombination in a haploid yeast strain carrying 99% identical alleles located on different chromosomes. The fate of the broken chromosome was followed in the whole cell population without imposing selective constraints. Our results show that all the cells were able to repair the broken chromosome by gene conversion. During the repair, the cells arrest in the cell cycle with a “dumbbell” configuration characteristic of G2/M-arrested cells. Surprisingly, although all the cells repaired the broken chromosome, 60% of them were unable to resume growth and to form colonies after the repair was completed. The low level of cell recovery was due to the 1% divergence between the alleles, but was not dependent on the function of the mismatch-repair system. Cell death, however, could be prevented by the presence of an alternative source of perfect homology located on a different chromosome.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002940000124
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  • 6
    Electronic Resource
    Electronic Resource
    Molecular cloning of SNM1, a yeast gene responsible for a specific step in the repair of cross-linked DNA (1989)
    Springer
    Molecular genetics and genomics 218 (1989), S. 64-71 
    Details
    ISSN: 1617-4623
    Keywords: Saccharomyces cerevisiae ; DNA repair ; Cross-link ; Transposon mapping ; Nitrogen mustard
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary We have isolated yeast gene SNM1 via complementation of sensitivity towards bi- and tri-functional alkylating agents in haploid and diploid yeast DNA repair-deficient snm1-1 mutants. Four independent clones of plasmid DNA containing the SNM1 locus were isolated after transformation with a YEp24-based yeast gene bank. Subcloned SNM1-containing DNA showed (i) complementation of the repair-deficiency phenotype caused by either one of the two different mutant alleles snm1-1 and snm1-2 ts; (ii) complementation in haploid and diploid yeast snm1-1 mutants by either single or multiple copies of the SNM1 locus; and (iii) that the SNM1 gene is at most 2.4 kb in size. Expression of SNM1 on the smallest subclone, however, was under the control of the GAL1 promotor. Gene size and direction of transcription was further verified by mutagenesis of SNM1 by Tn10-LUK transposon insertion. Five plasmids containing Tn10-LUK insertions at different sites of the SNM1-containing DNA were able to disrupt function of genomic SNM1 after gene transplacement. Correct integration of the disrupted SNM1::Tn10-LUK at the genomic site of SNM1 was verified via tetrad analysis of the sporulated diploid obtained after mating of the SNM1::Tn10-LUK transformant to a haploid strain containing the URA3 SNM1 wild-type alleles. The size of the poly(A)+ RNA transcript of the SNM1 gene is 1.1 kb as determined by Northern analysis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00330566
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  • 7
    Electronic Resource
    Electronic Resource
    Regulation of the RAD6 gene of Saccharomyces cerevisiae in the mitotic cell cycle and in meiosis (1986)
    Springer
    Molecular genetics and genomics 203 (1986), S. 538-543 
    Details
    ISSN: 1617-4623
    Keywords: Saccharomyces serevisiae ; DNA repair ; Cell cycle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary The regulation of the RAD6 gene at the mRNA level was investigated. The level of steady state RAD6 mRNA increases once every cell cycle, at late S/early G2. This stage is the one at which rad6 mutants arrest, as do wild-type cells exposed to hydroxyurea (HU) or methyl methanesulfonate (MMS), or cdc40 cells exposed to the restrictive temperature. This appears to be a repair-specific stage in the cell cycle. RAD6 mRNA levels increase when cells are treated with MMS, but this increase seems to be due to the arrest of the cells by MMS at the repair-specific stage; cells arrested at the same stage by HU or by the cdc40 lesion also show high levels of RAD6 mRNA. A much smaller increase in the level of RAD6 transcripts is seen following UV irradiation. During meiosis, RAD6 mRNA is more abundant before commitment to recombination. The differential increase of RAD6 mRNA during the S/G2 repair-specific stage of the cell cycle relates the RAD6 function to the normally occurring radioresistance found at this stage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00422083
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  • 8
    Electronic Resource
    Electronic Resource
    Effect of recF, recJ, recN, recO and ruv mutations on ultraviolet survival and genetic recombination in a recD strain of Escherichia coli K12 (1988)
    Springer
    Molecular genetics and genomics 212 (1988), S. 317-324 
    Details
    ISSN: 1617-4623
    Keywords: Escherichia coli ; Recombination ; DNA repair ; recD
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary DNA repair and recombination were investigated in a recD mutant of Escherichia coli which lacked the nuclease activity of the RecBCD enzyme. The resistance of this mutant to ultraviolet (UV) light was shown to be a function of recJ. A recD recJ double mutant was found to be more sensitive to UV radiation than a recB mutant, whereas recD and recJ single mutants were resistant. Recombination in conjugational crosses with Hfr donors was also reduced in recD recJ strains, but the effect was modest in comparison with the sensitivity to UV. Within certain limits, mutations in recF, recN, recO, lexA and ruv did not affect sensitivity to UV and recombination in a recD mutant any more than in a recD + strain. The possibility that recD and recJ provide overlapping activities, either of which can promote DNA repair and recombination in the absence of the other, is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00334702
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  • 9
    Electronic Resource
    Electronic Resource
    Regulation ofSNM1, an inducibleSaccharomyces cerevisiae gene required for repair of DNA cross-links (1996)
    Springer
    Molecular genetics and genomics 250 (1996), S. 162-168 
    Details
    ISSN: 1617-4623
    Keywords: DNA repair ; Regulation ; Gene fusion ; DRE element ; Saccharomyces cerevisiae
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The interstrand cross-link repair geneSNM1 ofSaccharomyces cerevisiae was examined for regulation in response to DNA-damaging agents. Induction ofSNM1-lacZ fusions was detected in response to nitrogen mustard, cis-platinum (II) diamine dichloride, UV light, and 8-methoxypsoralen + UVA, but not after heat-shock treatment or incubation with 2-dimethyl-aminoethylchloride, methylmethane sulfonate or 4-nitroquinoline-N-oxide. The promoter ofSNM1 contains a 15 bp motif, which shows homology to the DRE2 box of theRAD2 promoter. Similar motifs have been found in promoter regions of other damage-inducible DNA repair genes. Deletion of this motif results in loss of inducibility ofSNM1. Also, a putative negative up-stream regulation sequence was found to be responsible for repression of constitutive transcription ofSNM1. Surprisingly, no inducibility ofSNM1 was found after treatment with DNA-damaging agents in strains without an intactDUN1 gene, while regulation seems unchanged insad1 mutants.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02174175
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  • 10
    Electronic Resource
    Electronic Resource
    Molecular structure of the DNA cross-link repair gene SNM1(PSO2) of the yeast Saccharomyces cerevisiae (1992)
    Springer
    Molecular genetics and genomics 231 (1992), S. 194-200 
    Details
    ISSN: 1617-4623
    Keywords: Saccharomyces cerevisiae ; DNA repair ; Nitrogen mustard ; Interstrand cross-links ; Nucleotide sequence
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary A 3.2 kb yeast DNA fragment containing the DNA interstrand cross-link-specific repair gene SNM1 has been sequenced. Two genes were identified. SNM1 has an open reading frame of 1983 by and codes for a 661 amino acid protein. Hydrophobic analysis shows that the protein is most probably not directly membrane bound. The second gene, UGX1, has an open reading frame of 573 by coding for a polypeptide of 191 amino acid residues. The two genes are arranged head to head and share a 192 by divergent promoter region that contains three TATAAA motives, two for the SNM1 and one for the UGX1 locus. Gene UGX1 has no apparent influence on the sensitivity of the cell to cross-linking nitrogen mustard, as its disruption in wild type does not increase sensitivity to nitrogen mustard and the presence of multiple copies of the gene fails to complement the nitrogen mustard sensitivity phenotype of snm1 disruption mutants. Northern analysis revealed that the expression of SNM1 yields an average of 0.3 copies/cell of a 2.4 kb transcript, while expression of UGX1 yields higher levels of a 0.8 kb poly(A)+ RNA.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00279791
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