REPAIR OF UV‐IRRADIATED PLASMID DNA IN EXCISION REPAIR DEFICIENT MUTANTS OF Saccharomyces cerevisiae

Ikai, Kaori; Tano, Keizo; Ohnishi, Takeo; Nozu, Keiichi

doi:10.1111/j.1751-1097.1985.tb01557.x

Cited by 11 publications

(8 citation statements)

References 7 publications

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“…It is interesting to note here that identical results were obtained by other laboratories with radl-1 mutants and UV-incoming DNA (White and Sedgwick, 1985;Dominski and Jachymczyk, 1987). However, Ikai et al (1985) reported that the radl-2 mutant had a normal capacity to repair UVincoming DNA although the mutant was sensitive to UV. This may indicate that the repair of UVincoming DNA varies somewhat between different RADI alleles.…”

Section: Host Repair Processes Remove Uv Damage In the Incoming Dnasupporting

confidence: 88%

“…the plasmid survival was different from that found in the RAD+ host. The mutants rad2-6 (Ikai et al, 1985) and rad2 (Dominski and Jachymczyk, 1987) were able to repair UV-incoming DNA as well as the parental RA D + strains. Although different plasmid DNAs, transformation procedures and other experimental conditions were used, the differences between alleles should be further investigated.…”

Section: Host Repair Processes Remove Uv Damage In the Incoming Dnamentioning

confidence: 99%

“…In Saccharomyces cerevisiae, conflicting results have been reported. By using a protoplast transformation procedure, Ikai et al (1985) reported that excision repair deficient mutants (radf-2, rad2-6, rad3-2, rad4-4) were able to repair UV-irradiated YEpl3 plasmid DNA as well as the repair proficient strain. Jachymczyk (1984, 1987) reported also that rad2, rad3-2, rad4 and radlO mutants transformed by the protoplast procedure were able to repair UV-irradiated pBB29 plasmid DNA, although in contrast with Ikai et al (1985).…”

Section: Introductionmentioning

confidence: 99%

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REPAIR OF UV‐DAMAGED INCOMING PLASMID DNA IN Saccharomyces cerevisiae

Keszenman-Pereyra

1990

Photochem & Photobiology

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A whole-cell transformation assay was used for the repair of UV-damaged plasmid DNA in highly transformable haploid strains of Saccharomyces cerevisiae having different repair capabilities. Six rad alleles were selected from the three epistasis groups: rad 1-1 and rad2-1 from the RAD3 group, rad6-1 and rad18-2 from the RAD6 group, and rad52-1 and rad54-1 from the RAD52 group. Cells carrying single, double and triple rad alleles were transformed to uracil prototrophy by centromeric plasmid DNA (YCp19) modified in vitro with UV (254 nm). Surviving fractions were calculated as the number of transformants at each fluence relative to the number of transformants with unirradiated plasmid DNA. The sensitivity of incoming DNA in single rad mutants shows that most repair is carried out by excision repair and a RAD18-dependent process. In the rad52-1 host, the sensitivity of incoming DNA was intermediate between those found in RAD+ and rad2-1 hosts, suggesting the involvement of a recombinational repair process. Non-epistatic interactions were observed between rad alleles belonging to different epistasis groups. This provides validation for the classification of the three epistasis groups concerning the repair of chromosomal DNA for UV-incoming DNA. In both rad1-1 rad6-1 and rad1-1 rad18-2 rad54-1 hosts, the mean fluence for one lethal event corresponds approximately to one pyrimidine dimer per plasmid molecule, indicating that they are absolute repairless hosts for incoming DNA. A comparison between cell and plasmid survival reveals that there are differences in the repairability of both chromosomal and incoming DNA. The large effect of rad6-1 mutation on cell survival and the small effect on incoming DNA suggest that, in the RAD+ strain, the RAD6 product may be essential for the repair processes which act on chromosomal DNA, but not for those which act on incoming DNA. It is proposed that in yeasts postreplication repair of incoming DNA is limited to supercoiled molecules with 1-2 pyrimidine dimers that can initiate replication.

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Section: Host Repair Processes Remove Uv Damage In the Incoming Dnasupporting

confidence: 88%

Section: Host Repair Processes Remove Uv Damage In the Incoming Dnamentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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REPAIR OF UV‐DAMAGED INCOMING PLASMID DNA IN Saccharomyces cerevisiae

Keszenman-Pereyra

1990

Photochem & Photobiology

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“…Unfortunately, other rad3 mutant alleles were not examined by these authors. Similarly surprising results were reported by Ikai et al (101), who measured transformation frequencies for various rad mutants transfected with a UV-irradiated multicopy plasmid. They noted that, relative to a wild-type strain, transforma-tion was unaffected in the rad3-2 strain and also in radl-2, rad2-6, and rad44 strains.…”

Section: Plasmids To Monitor Nucleotide Excision Repairsupporting

confidence: 79%

“…White and Sedgwick (282) noted that the UV sensitivity of the rad3-2 strain reported by Dominski and Jachymczyk (41) was significantly less than that expected and suggested that the rad3-2 strain used by the latter authors may have accumulated suppressors. However, there is no obvious explanation for the results of Ikai et al (101), and the use of plasmids for probing the molecular biology of excision repair in S. cerevisiae may involve experimental artifacts that remain to be identified.…”

Section: Plasmids To Monitor Nucleotide Excision Repairmentioning

confidence: 99%

Deoxyribonucleic acid repair in the yeast Saccharomyces cerevisiae.

Friedberg¹

1988

Microbiological Reviews

179

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UV hypersensitivity of yeast linear plasmids

et al. 1994

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The Kluyveromyces linear plasmids pGKL1 and pGKL2, encoding killer activity, were efficiently cured by UV irradiation. This event was investigated in more detail by the use of the terminal protein (TP)-associated cytoplasmic linear plasmids, pJKL1 and pRKL2, with a selectable marker LEU2. This observation was compared with the UV effect on the nuclear plasmids pLS1 (telomere-associated linear form) and YCp121 (centromere-integrated circular form), indicating that the UV hypersensitivity was specific to the cytoplasmic plasmids. Using rad4 and wild-type strains of S. cerevisiae, both pJKL1 and the nuclear plasmids were found to respond not only to photoreactivation repair but also to excision repair of UV-induced DNA damage. Thus these DNA repair systems were functional for both the nuclear and cytoplasmic plasmids in yeast, and it was suggested that the UV hypersensitivity of cytoplasmic plasmids might have been caused by a defect in other repair systems or in the TP-primed replication. Possibly TP-associated Debaryomyces linear plasmids were also UV hypersensitive.

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REPAIR OF UV‐IRRADIATED PLASMID DNA IN EXCISION REPAIR DEFICIENT MUTANTS OF Saccharomyces cerevisiae

Cited by 11 publications

References 7 publications

REPAIR OF UV‐DAMAGED INCOMING PLASMID DNA IN Saccharomyces cerevisiae

REPAIR OF UV‐DAMAGED INCOMING PLASMID DNA IN Saccharomyces cerevisiae

Deoxyribonucleic acid repair in the yeast Saccharomyces cerevisiae.

UV hypersensitivity of yeast linear plasmids

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