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The pol3-t hyperrecombination phenotype and DNA damage-induced recombination in Saccharomyces cerevisiae Is RAD50 dependent (Articolo in rivista)
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- Label
- The pol3-t hyperrecombination phenotype and DNA damage-induced recombination in Saccharomyces cerevisiae Is RAD50 dependent (Articolo in rivista) (literal)
- Anno
- 2009-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1155/2009/312710 (literal)
- Alternative label
Galli A, Hafer K, Cervelli T, Schiestl RH (2009)
The pol3-t hyperrecombination phenotype and DNA damage-induced recombination in Saccharomyces cerevisiae Is RAD50 dependent
in Journal of Biomedicine and Biotechnology (Online)
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- Galli A, Hafer K, Cervelli T, Schiestl RH (literal)
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- Titolo
- The pol3-t hyperrecombination phenotype and DNA damage-induced recombination in Saccharomyces cerevisiae Is RAD50 dependent (literal)
- Abstract
- The DNA polymerase ? (POL3/CDC2) allele pol3-t of Saccharomyces cerevisiae has previously been shown to be sensitive to methylmethanesulfonate (MMS) and has been proposed to be involved in base excision repair. Our results, however, show that the pol3-t mutation is synergistic for MMS sensitivity with MAG1, a known base excision repair gene, but it is epistatic with rad50 ?, suggesting that POL3 may be involved not only in base excision repair but also in a RAD50 dependent function. We further studied the interaction of pol3-t with rad50 ? by examining their effect on spontaneous, MMS-, UV-, and ionizing radiation-induced intrachromosomal recombination. We found that rad50 ? completely abolishes the elevated spontaneous frequency of intrachromosomal recombination in the pol3-t mutant and significantly decreases UV- and MMS-induced recombination in both POL3 and pol3-t strains. Interestingly, rad50 ? had no effect on ?-ray-induced recombination in both backgrounds between 0 and 50Gy. Finally, the deletion of RAD50 had no effect on the elevated frequency of homologous integration conferred by the pol3-t mutation. RAD50 is possibly involved in resolution of replication forks that are stalled by mutagen-induced external DNA damage, or internal DNA damage produced by growing the pol3-t mutant at the restrictive temperature. (literal)
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