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  • DNA repair  (3)
  • Mutagen hyper-resistance  (3)
  • Thermoconditional DNA repair  (3)
  • MNNG  (2)
  • 1
    ISSN: 1432-0983
    Keywords: Mutagen hyper-resistance ; Yeast ; Base sequence ; Gene disruption
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary A multi-copy plasmid containing the SNQ3 gene confers hyper-resistance to 4-nitroquinoline-N-oxide (4NQO), Trenimon, MNNG, cycloheximide, and to sulfometuron methyl in yeast transformants. Restriction analysis, subcloning, and DNA sequencing revealed an open reading frame of 1950 bp on the SNQ3-containing insert DNA. Gene disruption and transplacement into chromosomal DNA yielded 4NQO-sensitive null mutants which were also more sensitive than the wild-type to Trenimon, cycloheximide, sulfometuron methyl, and MNNG. Hydropathic analysis showed that the SNQ3-encoded protein is most likely not membrane-bound, while the codon bias index points to low expression of the gene.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0983
    Keywords: Mutagen hyper-resistance ; Nitrogen mustard ; Saccharomyces cerevisiae
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary A screening of haploid yeast strains for enhanced resistance to nitrogen mustard (HN2) yielded a recessive mutant allele, hnm1, that conferred hyper-resistance (HYR) to HN2. Diploids, homo- or heterozygous for the HNM1 locus, exhibit normal wild-type like resistance while homozygosity for hnm1 leads to the phenotype HYR to HN2. The hnm1 mutation could be found in yeast strains proficient or deficient in different DNA repair systems. In these mostly HN2-sensitive haploid repair-deficient mutants, hnm1 acted as a partial suppressor of HN2 sensitivity. All isolated recessive mutations conferring hyper-resistance belonged to a single complementations group. The HYR to HN2 phenotype was maximally expressed in growing cells and was associated with reduced mutability by HN2. HNM1 most probably controls uptake of HN2 which would be impaired in the hnm1 mutants.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0983
    Keywords: Multi-copy plasmid ; Hyper-resistance ; 4-NQO ; MNNG ; Triaziquone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Screening of a multi-copy vector-based yeast genomic library in haploid cells of wild-type Saccharomyces cerevisiae yielded transformants hyper-resistant to various chemical mutagens. Genetical analysis of the yeast insert DNAs revealed three genes SNG1, SNQ2, and SNQ3 that confer the phenotype hyper-resistance to MNNG, to 4-NQO and triaziquone, and to mutagens 4-NQO, MNNG, and triaziquone, respectively. Integration of the gene disruption-constructs into the haploid yeast genome yielded viable null-mutants with a mutagen-sensitive phenotype. Thus, copy number of these non-essential yeast genes determines the relative resistance to certain chemical mutagens, with zero copies yielding a phenotype of mutagen sensitivity and multiple copies one of mutagen hyper-resistance, respectively.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0983
    Keywords: Saccharomyces cerevisiae ; Multiple mutants of DNA repair ; Sensitivity to nitrogen mustard and to radiation ; Thermoconditional DNA repair
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Three haploid yeast mutants (snm) sensitive or thermoconditionally sensitive to the DNA cross-linking agent nitrogen mustard (HN2) were crossed with four rad strains representing mutations in the three pathways of DNA dark repair. The resulting haploid double and triple mutant strains were tested for their sensitivity to UV, HN2 and HN1. From the observed epistatic or synergistic interactions of the combinations of mutant alleles we could derive the relation of the SNM1 and SNM2 genes to the postulated repair pathways. Alleles snm1-1 and snml-2 ts were found epistatic to genes of the rad3 group, whereas snm2-1 ts was epistatic to rad6. The snm1 and snm2 mutant alleles interacted synergistically. From these data it is concluded that the SNM1 gene product plays a cross-link specific role in excision repair while the SNM2 gene product may be involved in a system of error-prone repair.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0983
    Keywords: Yeast ; Thermoconditional DNA repair ; Mutagenesis ; Allelism test
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Of two mutant genes (snm1-2 ts and snm2-1 ts) conferring thermoconditional mutagen sensitivity in Saccharomyces cerevisiae one (snm2-1 ts) is shown to be centromere-linked. At the restrictive temperature this allele reduces UV-induced back mutation frequency of the ochre allele hiss-2 but has no influence on forward mutation at the CAN1 locus. Complementation tests and recombination analysis revealed snm2 ts to be allelic with rad5 (rev2).
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0983
    Keywords: Yeast ; GSH ; DNA alkylation ; MNNG
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The MNNG hyper-resistance of yeast transformants containing multiple copies of the SNQ3/YAP1 yeast gene is not caused by lowered MNNG activation due to depleted pools of glutathione. On the contrary, the SNQ3/YAP1-encoded protein stimulates production of GSH, apparently by promoter activation due to the AP-1 recognition element. Expression of at least one further gene, encoding a protein with a strong detoxifying activity, must also be stimulated to explain the MNNG hyper-resistance phenotype.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-0983
    Keywords: Yeast mutants ; Nitrogen mustard ; Thermoconditional DNA repair
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Selection of mutants of Saccharomyces cerevisiae sensitive to the DNA cross-linking agent nitrogen mustard (HN2) at two temperatures (23 °C and 36 °C) yielded two isolates with thermoconditionally enhanced (ts) sensitivity to the mutagen. Both were due to single recessive nuclear genes. Mutant allele snm1–2 ts showed mainly ts-sensitivity to HN2, whereas mutant allele snm2-1 ts conferred ts-sensitivity to HN2, half mustard (HN1) and UV. In temperature-shift experiments it was determined that the functions of SNM1 and SNM2 are needed for recovery within 6 to 7 h. after mutagen exposure during incubation at 23 °C on YEPD when HN2 and UV are applied. After HN1 treatment the SNM2 coded function is required for recovery for about 14 hrs. This possibly indicates a handling of UV- and HN2-induced lesions different from that of HN1-induced lesions.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Molecular genetics and genomics 231 (1992), S. 194-200 
    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
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  • 9
    ISSN: 1617-4623
    Keywords: Mutagen hyper-resistance ; 4-nitroquinolineN-oxide ; Yeast ; ATP-dependent permease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary The yeast gene SNQ2 confers hyper-resistance to the mutagens 4-nitroquinoline-N-oxide (4-NQO) and Triaziquone, as well as to the chemicals sulphomethuron methyl and phenanthroline when present in multiple copies in transformants of Saccharomyces cerevisiae. Subcloning and sequencing of a 5.5 kb yeast DNA fragment revealed that SNQ2 has an open reading frame of 4.5 kb. The putative encoded polypeptide of 1501 amino acids has a predicted molecular weight of 169 kDa and has several hydrophobic regions. Northern analysis showed a transcript of 5.5 kb. Haploid cells with a disrupted SNQ2 reading frame are viable. The SNQ2-encoded protein has domains believed to be involved in ATP binding and is likely to be membrane associated. It most probably serves as an ATP-dependent permease.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Molecular genetics and genomics 250 (1996), S. 162-168 
    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
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