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Indirect Suppression of Radiation Sensitivity of a recA Strain of Escherichia coli K12

  • David W. Mount
  • Anita C. Walker
  • Candace Kosel
Part of the Basic Life Sciences book series

Abstract

It has been shown previously that the radiation sensitivity of LexA strains of Escherichia coli K-12 can be suppressed by thermosensitive mutations (designated tsl) that are closely linked to the lexA locus. These are thought to be intragenic suppressors that reduce the activity of the diffusible product that gives rise to the LexAphenotype (Mount et al., 1973). When a recA mutation is crossed into a suppressed tsl strain, the extreme radiation sensitivity usually conferred by a recA mutation is considerably reduced without any detectable change in genetic recombination deficiency. Suppression of UV sensitivity depends upon the activity of the uvrA + product. We propose that at least part of the radiation sensitivity of a recA strain is due to a DNA repair defect that is different from inability to perform genetic exchanges and depends upon the presence of the lexA + product. We hypothesize that the lexA + product is a repressor of the synthesis of repair enzymes. In recA + cells with DNA lesions, repressor is inactivated leading to enzyme induction but this does not occur in recA cells. tsl mutations inactivate repressor leading to constitutive enzyme synthesis and bypassing the need for recA + product to inactivate the lexA + product.

Keywords

Repair Enzyme Genetic Recombination Radiation Sensitivity Pyrimidine Dimer Diffusible Product 
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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Copyright information

© Plenum Press, New York 1975

Authors and Affiliations

  • David W. Mount
    • 1
  • Anita C. Walker
    • 2
  • Candace Kosel
    • 1
  1. 1.Department of Microbiology,College of MedicineUniversity of ArizonaTucsonUSA
  2. 2.Roche Institute of Molecular BiologyNutleyUSA

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