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Repair of UV-irradiated plasmid DNA in a Saccharomyces cerevisiae rad3 mutant deficient in excision-repair of pyrimidine dimers

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Summary

The repair of UV-irradiated DNA of plasmid pBB29 was studied in an incision-defective rad3-2 strain of Saccharomyces cerevisiae and in a uvrA6 strain of Escherichia coli by the measurement of cell transformation. Plasmid pBB29 used in these experiments contained as markers the DNA of nuclear yeast gene LEU-2 and DNA of the bacterial plasmid pBR327 with resistance to Tet and Amp enabling simultaneous screening of transformant cells in both microorganisms.

We found that the yeast rad3-2 mutant, deficient in incision of UV-induced pyrimidine dimers in nuclear DNA, was fully capable of repairing such lessions in plasmid DNA. The repair efficiency was comparable to that of the wild-type cells. The E. coli uvrA6 mutant, deficient in a specific nuclease for pyrimidine dimer excision from chromosomal DNA, was unable to repair UV-damaged plasmid DNA. The difference in repair capacity between the uvrA6 mutant strain and the wild-type strain was of several thousand-fold.

It seems that the rad3 mutation, which confers deficiency in the DNA excision-repair system in yeast, is limited only to the nuclear DNA.

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Communicated by F. Kaudewitz

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Dominski, Z., Jachmczyk, W.J. Repair of UV-irradiated plasmid DNA in a Saccharomyces cerevisiae rad3 mutant deficient in excision-repair of pyrimidine dimers. Molec. Gen. Genet. 193, 167–171 (1984). https://doi.org/10.1007/BF00327432

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  • DOI: https://doi.org/10.1007/BF00327432

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