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Genetic Analysis of Error-Prone Repair Systems in Saccharomyces cerevisiae

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DNA Repair and Mutagenesis in Eukaryotes

Part of the book series: Basic Life Sciences ((BLSC,volume 15))

Summary

The manner in which ultraviolet induced mutagenesis occurs in yeast is discussed and compared with ultraviolet mutagenesis in Escherichia coli. In both excision proficient and excision deficient strains of Escherichia coli, mutations arise as the square of the ultraviolet dose whereas in yeast, mutations arise as the square of the dose only in excision proficient strains. In excision defective yeast strains, mutations induced by ultraviolet arise with linear kinetics. Ultraviolet irradiation of excision proficient haploid or diploid yeast during G1 results in fixation of mutation in both DNA strands prior to DNA replication, whereas in excision defective strains, the frequency of two strand mutations is very low, and the frequency of one strand mutations and mutations appearing in the second post irradiation mitotic division is increased. All of these results in yeast can be explained by error prone excision repair of two closely spaced dimers in opposite DNA strands in excision proficient strains and occasional error prone filling of postreplication gaps, which are not usually overlapping daughter strand gaps, in excision defective yeast. The dependence of UV mutagenesis on functional RAD6, REV3, CDC8 and MMS3 gene functions is discussed. The MMS3 function appears to be required for UV mutagenesis in a./α diploids but is dispensible in a /a or α/α diploids and in haploids, suggesting that differences exist between error prone repair processes in haploids, a/a, α/α diploids vs. a/α diploids.

Alkylating agent induced mutations in yeast depend on functional RAD6, RAD9, RAD51 and RAD52 genes. Different alleles of the RAD52 locus differ in their effects on ethyl methanesulfonate induced mutations of different sites within the same gene. Misreplication of O6-alkyl guanine probably does not account for most of the mutations induced by alkylating agents in yeast: instead, they probably result from RAD6-dependent error prone repair of gaps opposite O6-alkyl guanine. Error prone repair pathways for repair of radiation damage differ in some respects from error prone repair of damage induced by chemical agents.

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Authors and Affiliations

  1. Department of Radiation Biology and Biophysics, School of Medicine, Rochester, New York, 14627, USA

    Louise Prakash

  2. Department of Biology, University of Rochester, Rochester, New York, 14627, USA

    Satya Prakash

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  1. Louise Prakash
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Editors and Affiliations

  1. Oak Ridge National Laboratories, Oak Ridge, Tennessee, USA

    W. M. Generoso

  2. National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA

    M. D. Shelby  & F. J. de Serres  & 

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© 1980 Plenum Press, New York

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Prakash, L., Prakash, S. (1980). Genetic Analysis of Error-Prone Repair Systems in Saccharomyces cerevisiae . In: Generoso, W.M., Shelby, M.D., de Serres, F.J. (eds) DNA Repair and Mutagenesis in Eukaryotes. Basic Life Sciences, vol 15. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-3842-0_9

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  • DOI: https://doi.org/10.1007/978-1-4684-3842-0_9

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