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Genetic Exchanges Induced by Structural Damage in Nonreplicating Phage λ DNA

  • P. Howard-Flanders
  • P.-F. Lin
  • E. Bardwell
Part of the Basic Life Sciences book series

Abstract

Genetic recombination between irradiated λ phage and the unirradiated λ prophage in homoimmune lysogens has been studied under conditions in which phage DNA replication and repair were controlled. The λ phage were exposed to one of three treatments before infecting the lysogens: (a) 254-nm light, which produces pyrimidine dimers and other photoproducts; (b) 313-nm light with acetopheneone D, which produces thymine dimers and a different spectrum of other photoproducts; (c) 360-nm light with trimethylpsoralen, which produces monoadducts and cross-links. With both replication and excision-repair of the damaged phage DNA blocked, treatment b (acetophenone D) caused no significant increase in recombination, indicating that thymine dimers do not cause recombination if the DNA in which they are contained is not replicated. Treatment a (254 nm), producing the same total number of pyrimidine dimers, caused a marked increase in recombination. This indicates that photoproducts other than pyrimidine dimers produced by 254-nm light can cause recombination in the absence of replication. Treatment c (psoralen) caused a marked increase in recombination in wild type but not in uvrA and uvrB mutants. The frequency of recombination in two-factor crosses varied with marker separation in such a way as to suggest that cross-links can act over distances of at least 5% of the λ genome to cause exchanges between pairs of relatively closely spaced markers. The psoralen photo cross-links and monoadducts initiate recombination only following the action of excision enzymes, which appear to release one arm of each cross-link, producing a gap with free strand ends. It may be these strand ends which induce recombination. The action at a distance of 5% of the λ genome may reflect heteroduplex formation and the subsequent reduction to homozygosity of mismatched base pairs at genetic markers. Recombination between closely spaced markers in the P gene is reduced in strains carrying polA.

Keywords

Pyrimidine Dimer Mismatched Base Pair Thymine Dimer Marker Separation States Public Health Service Grant 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. Blanco, M. and Devoret, R. (1973). Mutat. Res. 17, 293–305.PubMedCrossRefGoogle Scholar
  2. Cole, R. S. (1970). Biochim. Biophys. Acta 217, 30–39.PubMedGoogle Scholar
  3. Cole, R. S. (1971). Biochim. Biophys. Acta 254, 30–39.PubMedGoogle Scholar
  4. Cole, R. S. (1973). Proc. Nat. Acad. Sci U.S.A. 70, 1064–1068.CrossRefGoogle Scholar
  5. Fincham, J. R. S. and Holliday, R. (1970). Mol. Gen. Genet. 109, 309–322.PubMedCrossRefGoogle Scholar
  6. Glickman, B. W., van Sluis, C. A., Heijneker, H. L. and Rorsch, A. (1973). Mol. Gen. Genet. 124, 69–82.PubMedCrossRefGoogle Scholar
  7. Grossman, L. and Rogers, E. (1968). Biochem. Biophys. Res. Commun. 33, 975–983.PubMedCrossRefGoogle Scholar
  8. Hart, M. G. R. and Ellison, J. (1970). J. Gen. Virol. 8, 197–208.PubMedCrossRefGoogle Scholar
  9. Holliday, R. (1964). Genet. Res. 5, 282–304.CrossRefGoogle Scholar
  10. Howard-Flanders, P. and Lin, P.-F. (1973). Genetics 73 (suppl.), 85–90.PubMedGoogle Scholar
  11. Jacob, F. and Wollman, E. L. (1955). Ann. Inst. Pasteur, 88, 724–749.Google Scholar
  12. Jacob, F. and Wollman, E. L. (1963). Cold Spring Harbor Symp. Quant. Biol. 18, 101–121.CrossRefGoogle Scholar
  13. Kohn, K. W., Steigbigel, N. H. and Spears, C. L. (1965). Proc. Nat. Acad. Sci. U.S.A. 53, 1154–1161.CrossRefGoogle Scholar
  14. Konrad, E. B. and Lehman, I. R. (1974). Proc. Nat. Acad. Set U.S.A. 71, 2048–2051.CrossRefGoogle Scholar
  15. Manney, T. R. and Mortimer, R. K. (1964) Science 143, 581–583.CrossRefGoogle Scholar
  16. Meistrich, M. L. and Lamola, A. A. (1972). J. Mol. Biol. 66, 83–95.PubMedCrossRefGoogle Scholar
  17. Meselson, M. (1964). J. Mol. Biol. 9, 734–745.PubMedCrossRefGoogle Scholar
  18. Rupp, W. D., Wilde, C. E. and Reno, D. L. (1971). J. Mol. Biol. 61, 25–44.PubMedCrossRefGoogle Scholar
  19. Setlow, R. B. and Carrier, W. L. (1966). J. Mol. Biol. 17, 237–254.PubMedCrossRefGoogle Scholar
  20. Smith, K. C. (1967). In Radiation Research (Silini, G., ed.), p. 756. Wiley, New York.Google Scholar
  21. Stahl, F. W., McMilin, K. D., Stahl, M. M., Malone, R. E., Nozu, Y. and Russo, V.E.A. (1972a). J. Mol. Biol. 68, 49–55.CrossRefGoogle Scholar
  22. Stahl, F. W., McMilin, K. D., Stahl, M. M. and Nozu, Y. (1972b). Proc. Nat. Acad. Sci. U.S.A. 69, 3598–3601.CrossRefGoogle Scholar
  23. Vargahese, A. J. and Wang, S. Y. (1968). Science, 160, 186–187.CrossRefGoogle Scholar
  24. White, R. L. and Fox, M. S. (1974). Proc. Nat. Acad. Sci. U.S.A. 71, 1544–1548.CrossRefGoogle Scholar
  25. Yamamoto, N. (1967). Biochem. Biophys. Res. Commun. 27, 263–269.PubMedCrossRefGoogle Scholar
  26. Zimmerman, F. K. (1971). Mutat. Res. 11, 327–337.Google Scholar

Copyright information

© Plenum Press, New York 1975

Authors and Affiliations

  • P. Howard-Flanders
    • 1
    • 2
  • P.-F. Lin
    • 1
    • 2
  • E. Bardwell
    • 1
    • 2
  1. 1.Department of Molecular Biophysics and BiochemistryYale UniversityNew HavenUSA
  2. 2.Department of Therapeutic RadiologyYale UniversityNew HavenUSA

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