Perturbation of the SOS Response of Escherichia coli by Plasmids Carrying Truncated recA Genes

  • S. G. Sedgwick
  • G. T. Yarranton
Part of the NATO Advanced Study Institutes Series book series (NSSA, volume 40)


Several models for the regulation of E. coli recA + gene expression and induction of qS functions envisage that the recA + gene is repressed by the lexA + gene product. Positive control is thought to occur by “activation” of the basal level of recA + protein so that it in2ctivates both lexA + protein and the repressors of the SOS functions2-5. Such models predict that an excess of recA promotor-operato sequences would titrate lexA + repression of the chromosomal recA + gene2. The result would be escape synthesis of recA + protein,and perhaps easier inducibility of SOS functions.To test these naive predictions recA control sequences were introduced into E. coli by transformation with pBR322 derivatives, carr/ing the recA control sequence and 100%, 75% and 20% of the recA + structural gene (fig.l) pgR1453 and pDR1461 were very generously supplied by Dr. Dean Rupp6.


recA Protein lexA Gene Expectation Transformation pBR322 Site pBR322 Derivative 


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    M. Radman,in: “Molecular and environmental aspects of mutagenesis”, L. Prakash, F. Sherman, M. Miller, C. Lawrence and H.W. Tabor, eds., C.C. Thomas, Springfield, Ill. pp128142 (1974)Google Scholar
  2. 2.
    K. McEntee, Proc. Nat. Acad. Sci. 74: 5275-5279 (1977)Google Scholar
  3. 3.
    L. Gudas and D. Mount, Proc. Nat. Acad. Sci. 74: 5280–5284 (1977)CrossRefGoogle Scholar
  4. 4.
    P.T. Emmerson and S.C. West, Molec. Gen. Genet. 155: 77–85 (1977)Google Scholar
  5. 5.
    S.G. Sedgwick, A. Levine and A. Bailone, Molec. Gen. Genet. 160: 267–276 (1978)Google Scholar
  6. 6.
    A. Sancar and W.D. Rupp, Proc. Nat. Acad. Sci. 76: 3144–3148 (1979)CrossRefGoogle Scholar
  7. 7.
    A. GOZe and S.G. Sedgwick, Mutation Res. 52: 323–331 (1978)Google Scholar
  8. 8.
    J.W. Little, Molec. Gen. Genet. 177: 13–22 (1979) Google Scholar
  9. 9.
    J. Dorsch, J. Greenberg, and M.H.L. Green, Genet. Res.15:87–97 (1970)Google Scholar
  10. 10.
    M. Castellazzi, J. George and G. Buttin, Molec. Gen. Genet. 119: 153–174 (1972)Google Scholar
  11. 11.
    J. Do,n:h, M.H.L. Green and J. Greenberg, J. Bacteriol. 96: 1704–1710 (1968)Google Scholar
  12. 12.
    T. Ogawa, H. Wabiko, T. Tsurimoto, T. Tsurimoto, T. Horii, H. Masukata and H. Ogawa, Cold Spring Harbour Symp. Quant. Biol. 43: 909–915 (1978)CrossRefGoogle Scholar
  13. 13.
    E.M. Witkin, Proc. Nat. Acad. Sci. 71: 1930–1934 (1974)Google Scholar

Copyright information

© Plenum Press, New York 1981

Authors and Affiliations

  • S. G. Sedgwick
    • 1
  • G. T. Yarranton
    • 1
  1. 1.Genetics DivisionNational Institute for Medical ResearchLondonUK

Personalised recommendations