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  • Nitrogen mustard  (4)
  • Formaldehyde  (3)
  • Hyper-resistance  (2)
  • 1
    Electronic Resource
    Electronic Resource
    A recessive mutant allele of the HNM1 gene of Saccharomyces cerevisiae is responsible for hyper-resistance to nitrogen mustard (1990)
    Springer
    Current genetics 18 (1990), S. 187-192 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00318378
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  • 2
    Electronic Resource
    Electronic Resource
    Isolation and characterization of additional genes influencing resistance to various mutagens in the yeast Saccharomyces cerevisiae (1992)
    Springer
    Current genetics 21 (1992), S. 319-324 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00351689
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  • 3
    Electronic Resource
    Electronic Resource
    Isolation and characterization of yeast mutants with thermoconditional sensitivity to the bifunctional alkylating agent nitrogen mustard (1981)
    Springer
    Current genetics 4 (1981), S. 145-149 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00365693
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  • 4
    Electronic Resource
    Electronic Resource
    Hyperresistance to formaldehyde of Saccharomyces cerevisiae seems not to be correlated with the formation and removal of DNA protein cross-links (1988)
    Springer
    Current genetics 13 (1988), S. 125-128 
    Details
    ISSN: 1432-0983
    Keywords: Formaldehyde ; DNA-protein cross-links ; Repair ; Saccharomyces cerevisiae ; Hyperresistance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary The formation and removal of formaldehyde-mediated DNA protein cross-linking was measured by CsCI density gradient analysis in yeast strains of differing resistance to formaldehyde. Wild-type cells and transformants made hyperresistant to formaldehyde by a multi-copy vector containing the yeast SFA gene were specifically labeled in their DNA and incubated in the presence of formaldehyde. Treatment with formaldehyde lead to the formation of equal amounts of DNA protein cross-links; subsequent liquid holding of cells for 24 h resulted in the removal of nearly all DNA protein crosslinks regardless of the original formaldehyde resistance status of the strains.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00365646
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  • 5
    Electronic Resource
    Electronic Resource
    Overexpression ofADH1 confers hyper-resistance to formaldehyde inSaccharomyces cerevisiae (1996)
    Springer
    Current genetics 29 (1996), S. 437-440 
    Details
    ISSN: 1432-0983
    Keywords: Yeast ; Formaldehyde ; Hyper-resistance ; Alcohol dehydrogenase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract In an attempt to clone genes involved in resistance to formaldehyde we have screened a genomic library based on the episomal plasmid YEp24 for the ability to increase resistance to formaldehyde in a wild-type strain. In addition toSFA, the gene encoding the formaldehyde dehydrogenase Adh5, an enzyme most potent in formaldehyde de-toxification, we isolated a second plasmid that conferred a less pronounced but significant hyper-resistance to formaldehyde. Its passenger DNA contained the geneADH1, encoding alcohol dehydrogenase 1 (EC 1.1.1.1), which could be shown to be responsible for the observed hyper-resistance phenotype. Construction of anadh1-0 mutant revealed that yeast lacking a functionalADH1 gene is sensitive to formaldehyde. While glutathione is essential for Adh5-mediated formaldehyde de-toxification, Adh1 reduced formaldehyde best in the absence of this thiol compound. Evidence is presented that formaldehyde is a substrate for Adh1 in vivo and in vitro and that its cellular de-toxification employs a reductive step that may yield methanol.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02221511
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  • 6
    Electronic Resource
    Electronic Resource
    Genetic characterization of hyperresistance to formaldehyde and 4-nitroquinoline-N-oxide in the yeast Saccharomyces cerevisiae (1988)
    Springer
    Molecular genetics and genomics 211 (1988), S. 260-265 
    Details
    ISSN: 1617-4623
    Keywords: Mutagen resistance ; Yeast ; Formaldehyde ; 4-Nitroquinoline-N-oxide ; Multi-copy plasmids
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary The hyperresistance to 4-nitroquinoline-N-oxide (4-NQO) and formaldehyde (FA) of yeast strains transformed with the multi-copy plasmids pAR172 and pAR184, respectively, is due to the two genes, SNQ and SFA, which are present on these plasmids. Restriction analysis revealed the maximal size of SFA as 2.7 kb and of SNQ as 2.2 kb, including transcription control elements. The presence of the smallest 2.7 kb subclone carrying SFA increased hyperresistance to formaldehyde fivefold over that of the original pAR184 isolate. No such increase in hyperresistance to 4-NQO was seen with the smaller subclones of the pAR172 isolate. Disruption of the SFA gene led to a threefold increase in sensitivity to FA as compared with the wild type. Expression of gene SNQ introduced on a multi-copy vector into haploid yeast mutants rad2, rad3, and snm1 did not complement these mutations that block excision repair.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00330602
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  • 7
    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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  • 8
    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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