Relationships Among Repair, Mutagenesis, and Survival: Overview

  • Evelyn M. Witkin
Part of the Basic Life Sciences book series


In genetically damaged cells, the pathways of survival, mutagenesis, and repair are inseparable. An irradiated or chemically treated cell, having sustained potentially lethal damage to its DNA, may or may not survive. Surviving, it may or may not have kept intact its store of genetic information. The fate of such a cell depends in part upon the nature and degree of primary DNA damage, in part upon the DNA repair systems available to the cell which are capable of neutralizing the damage, and to an important extent also upon the internal and external environmental factors which determine how effectively repair mechanisms can operate. A surviving cell may have undergone a mutation either because an unrepaired DNA lesion has generated a replication error or because an error-prone repair system has changed the base sequence in the course of restoring a viable DNA structure (see Witkin, 1969; Bridges, 1969; Kondo, 1973; Doudney, 1974).


Repair System Pyrimidine Dimer Repair Synthesis Post Replication Repair Postreplication Repair 
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  1. Boyle, J. M., Patterson, M. C. and Setlow, R. B. (1970). Nature 226, 708–710.PubMedCrossRefGoogle Scholar
  2. Bridges, B. A. (1969). Ann. Rev. Nuci Sci. 19, 139–178.CrossRefGoogle Scholar
  3. Cooper, P. K. and Hanawalt, P. C. (1972). J. Mol. Biol. 67, 1–10.PubMedCrossRefGoogle Scholar
  4. Doudney, C. 0. (1975). In Photochemistry and Photobiology of Nucleic Acids, ed. S. Wang, Academic Press, New York, in press.Google Scholar
  5. Kanner, L. and Hanawalt, P. (1970). Biochem, Biophys. Res. Commun. 39, 149–155.CrossRefGoogle Scholar
  6. Kondo, S. (1973). Genetics SuppL 73, 109–122.Google Scholar
  7. Lieb, M. (1961). Z. Vererbungs 192, 416–429.CrossRefGoogle Scholar
  8. Mount, D. W., Low, K. B. and Edmiston, S J. (1972). J. Bacteriol. 112, 886–893.PubMedGoogle Scholar
  9. Nishioka, H. and Doudney, C. 0. (1969). Mutat. Res. 8, 215–228.Google Scholar
  10. Rupp, W. D. and Howard-Flanders, P. (1968). J. Mol. Biol. 31, 291–304.PubMedCrossRefGoogle Scholar
  11. Rupp, W. D., Wilde, C. E., III, Reno, D. L. and Howard-Flanders, P. (1971). J. Mol. Biol. 61, 25–44.PubMedCrossRefGoogle Scholar
  12. Smith, K. C. and Meun, D. H. C. (1970). J MoL Biol. 51, 459–472.PubMedCrossRefGoogle Scholar
  13. Witkin, E. M. (1961). J. CelL Comp. PhysioL 58 (Suppl. 1), 135–144.PubMedCrossRefGoogle Scholar
  14. Witkin, E. M. (1967). Brookhaven Symp. Biol. 20, 17–55.Google Scholar
  15. Witkin, E. M. (1969). Ann. Rev. MicrobioL 23, 487–514.CrossRefGoogle Scholar
  16. Youngs, D. A. and Smith, K. C. (1973). J. BacterioL 116, 175–182.PubMedGoogle Scholar

Copyright information

© Plenum Press, New York 1975

Authors and Affiliations

  • Evelyn M. Witkin
    • 1
  1. 1.Department of Biological Sciences, Douglas CollegeRutgers UniversityNew BrunswickUSA

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