A Saccharomyces cerevisiae phleomycin-sensitive mutant, phl40, is defective in the RAD6 DNA repair gene

1996 ◽  
Vol 42 (12) ◽  
pp. 1263-1266 ◽  
Author(s):  
Chuan Hua He ◽  
Jean-Yves Masson ◽  
Dindial Ramotar
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Repair ◽  
Anticancer Agent ◽  
Radiation Treatment ◽  
Dna Lesions ◽  
Exact Nature ◽  
Repair Gene ◽  
Yeast Saccharomyces Cerevisiae ◽  
Dna Repair Gene ◽  
Cellular Dna

The antibiotic bleomycin is used as an anticancer agent for treating a variety of tumours. The antitumour effect of bleomycin is related to its ability to produce lesions such as apurinic/apyrimidinic sites and single- and double-strand breaks in the cellular DNA. Phleomycin is a structurally related form of bleomycin, but it is not used as an anticancer agent. While phleomycin can also damage DNA, neither the exact nature of these DNA lesions nor the cellular process that repairs phleomycin-induced DNA lesions is known. As a first step to understand how eukaryotic cells provide resistance to phleomycin, we used the yeast Saccharomyces cerevisiae as a model system. Several phleomycin-sensitive mutants were generated following γ-radiation treatment and among these mutants, phl40 was found to be the most sensitive to phleomycin. Molecular analysis revealed that the mutant phl40 harbored a mutation in the DNA repair gene RAD6. Moreover, a functional copy of the RAD6 gene restored full phleomycin resistance to strain phl40. Our findings indicate that the RAD6 protein is essential for yeast cellular resistance to phleomycin.Key words: yeast, phleomycin, DNA repair, RAD6.

scholarly journals The essential DNA polymerases delta and epsilon are involved in repair of UV-damaged DNA in the yeast Saccharomyces cerevisiae.

1999 ◽  
Vol 46 (2) ◽  
pp. 289-298 ◽  
Author(s):  
A Hałas ◽  
Z Policińska ◽  
H Baranowska ◽  
W J Jachymczyk
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Repair ◽  
Uv Irradiation ◽  
Dna Polymerases ◽  
Relative Molecular Mass ◽  
Yeast Saccharomyces Cerevisiae ◽  
Strand Breaks ◽  
Single Strand Breaks ◽  
Mutant Strains ◽  
Cellular Dna

We have studied the ability of yeast DNA polymerases to carry out repair of lesions caused by UV irradiation in Saccharomyces cerevisiae. By the analysis of postirradiation relative molecular mass changes in cellular DNA of different DNA polymerases mutant strains, it was established that mutations in DNA polymerases delta and epsilon showed accumulation of single-strand breaks indicating defective repair. Mutations in other DNA polymerase genes exhibited no defects in DNA repair. Thus, the data obtained suggest that DNA polymerases delta and epsilon are both necessary for DNA replication and for repair of lesions caused by UV irradiation. The results are discussed in the light of current concepts concerning the specificity of DNA polymerases in DNA repair.

Failure to induce a DNA repair gene, RAD54, in Saccharomyces cerevisiae does not affect DNA repair or recombination phenotypes

1989 ◽  
Vol 9 (8) ◽  
pp. 3314-3322
Author(s):  
G M Cole ◽  
R K Mortimer
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Damage ◽  
Dna Repair ◽  
Constitutive Expression ◽  
Inducible Promoter ◽  
Positive Control ◽  
Repair Gene ◽  
Dna Damaging Agents ◽  
Dna Repair Gene ◽  
Mating Type Switching

The Saccharomyces cerevisiae RAD54 gene is transcriptionally regulated by a broad spectrum of DNA-damaging agents. Induction of RAD54 by DNA-damaging agents is under positive control. Sequences responsible for DNA damage induction (the DRS element) lie within a 29-base-pair region from -99 to -70 from the most proximal transcription start site. This inducible promoter element is functionally separable from a poly(dA-dT) region immediately downstream which is required for constitutive expression. Deletions which eliminate induction of RAD54 transcription by DNA damage but do not affect constitutive expression have no effect on growth or survival of noninducible strains relative to wild-type strains in the presence of DNA-damaging agents. The DRS element is also not required for homothallic mating type switching, transcriptional induction of RAD54 during meiosis, meiotic recombination, or spontaneous or X-ray-induced mitotic recombination. We find no phenotype for a lack of induction of RAD54 message via the damage-inducible DRS, which raises significant questions about the physiology of DNA damage induction in S. cerevisiae.

scholarly journals Regulation of the Saccharomyces cerevisiae DNA repair gene RAD16

1995 ◽  
Vol 23 (10) ◽  
pp. 1679-1685 ◽  
Author(s):  
D. d. Bang ◽  
V. Timmermans ◽  
R. Verhage ◽  
A. M. Zeeman ◽  
P. van de Putte ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Repair ◽  
Repair Gene ◽  
Dna Repair Gene

scholarly journals Repair of UV damage in plants by nucleotide excision repair: Arabidopsis UVH1 DNA repair gene is a homolog of Saccharomyces cerevisiae Rad1

2000 ◽  
Vol 21 (6) ◽  
pp. 519-528 ◽  
Author(s):  
Zongrang Liu ◽  
Gazi Showkat Hossain ◽  
Maria A. Islas-Osuna ◽  
David L. Mitchell ◽  
David W. Mount
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Repair ◽  
Nucleotide Excision Repair ◽  
Excision Repair ◽  
Uv Damage ◽  
Repair Gene ◽  
Dna Repair Gene ◽  
Nucleotide Excision

scholarly journals A modified fluctuation assay reveals a natural mutator phenotype that drives mutation spectrum variation within Saccharomyces cerevisiae

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Pengyao Jiang ◽  
Anja R Ollodart ◽  
Vidha Sudhesh ◽  
Alan J Herr ◽  
Maitreya J Dunham ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Repair ◽  
De Novo ◽  
Genetic Mutation ◽  
Mutation Spectrum ◽  
Mutation Rates ◽  
Complementation Test ◽  
Repair Gene ◽  
Dna Repair Gene ◽  
Mutator Allele

Although studies of Saccharomyces cerevisiae have provided many insights into mutagenesis and DNA repair, most of this work has focused on a few laboratory strains. Much less is known about the phenotypic effects of natural variation within S. cerevisiae's DNA repair pathways. Here, we use natural polymorphisms to detect historical mutation spectrum differences among several wild and domesticated S. cerevisiae strains. To determine whether these differences are likely caused by genetic mutation rate modifiers, we use a modified fluctuation assay with a CAN1 reporter to measure de novo mutation rates and spectra in 16 of the analyzed strains. We measure a 10-fold range of mutation rates and identify two strains with distinctive mutation spectra. These strains, known as AEQ and AAR, come from the panel's 'Mosaic beer' clade and share an enrichment for C>A mutations that is also observed in rare variation segregating throughout the genomes of several Mosaic beer and Mixed origin strains. Both AEQ and AAR are haploid derivatives of the diploid natural isolate CBS 1782, whose rare polymorphisms are enriched for C>A as well, suggesting that the underlying mutator allele is likely active in nature. We use a plasmid complementation test to show that AAR and AEQ share a mutator allele in the DNA repair gene OGG1, which excises 8-oxoguanine lesions that can cause C>A mutations if left unrepaired.

The DNA repair gene PSO3 of Saccharomyces cerevisiae belongs to the RAD3 epistasis group

1992 ◽  
Vol 21 (1) ◽  
pp. 85-90 ◽  
Author(s):  
Mara S. Benfato ◽  
Martin Brendel ◽  
Jo�o A. P. Henriques
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Repair ◽  
Repair Gene ◽  
Dna Repair Gene

scholarly journals Conserved pattern of antisense overlapping transcription in the homologous human ERCC-1 and yeast RAD10 DNA repair gene regions.

1989 ◽  
Vol 9 (4) ◽  
pp. 1794-1798 ◽  
Author(s):  
M van Duin ◽  
J van Den Tol ◽  
J H Hoeijmakers ◽  
D Bootsma ◽  
I P Rupp ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Repair ◽  
Excision Repair ◽  
Antisense Transcription ◽  
Human Cells ◽  
Repair Gene ◽  
Naturally Occurring ◽  
Dna Repair Gene ◽  
Evolutionarily Conserved ◽  
Overlapping Transcription

We report that the genes for the homologous Saccharomyces cerevisiae RAD10 and human ERCC-1 DNA excision repair proteins harbor overlapping antisense transcription units in their 3' regions. Since naturally occurring antisense transcription is rare in S. cerevisiae and humans (this is the first example in human cells), our findings indicate that antisense transcription in the ERCC-1-RAD10 gene regions represents an evolutionarily conserved feature.

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