Skip to main content
PMC home page
Proceedings of the National Academy of Sciences of the United States of America logoLink to Proceedings of the National Academy of Sciences of the United States of America
. 1984 Dec;81(23):7539–7543. doi: 10.1073/pnas.81.23.7539

Involvement of the activated form of RecA protein in SOS mutagenesis and stable DNA replication in Escherichia coli.

E M Witkin, T Kogoma
PMCID: PMC392182  PMID: 6390441

Abstract

DNA damage activates RecA protein of E. coli to a form (RecA*) that promotes proteolytic cleavage of LexA protein, the repressor of at least 17 DNA damage-inducible genes, resulting in expression of the SOS response. In addition to this known role, RecA* performs another function necessary for expression of SOS mutagenesis [Blanco, M., Herrera, G., Collado, P., Rebollo, J. & Botella, L. M. (1982) Biochimie 64, 633-636]. The additional role of RecA* could be (i) cleavage of another repressor, (ii) proteolytic processing of one or more proteins, or (iii) mechanistic interaction with DNA or with one or more other proteins. We describe experiments designed to test the first possibility. Our results suggest that neither SOS mutator activity nor ultraviolet mutagenesis requires induction by RecA* of any gene(s) outside the LexA regulon and that the additional role of RecA* is not cleavage of another repressor. We show that stable DNA replication, another DNA damage-inducible function [Kogoma, T., Torrey, T. A. & Connaughton, M. J. (1979) Mol. Gen. Genet. 176, 1-9], shares with SOS mutagenesis the requirement for RecA* activity, even in a strain constitutively expressing all LexA-controlled genes. In this strain, conditions that activate RecA initiate expression of stable DNA replication in the presence of chloramphenicol, without an intervening period of protein synthesis. We conclude that the additional function of RecA* in stable DNA replication is not another antirepressor activity.

Full text

PDF
7543

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. BURTON K. A study of the conditions and mechanism of the diphenylamine reaction for the colorimetric estimation of deoxyribonucleic acid. Biochem J. 1956 Feb;62(2):315–323. doi: 10.1042/bj0620315. [DOI] [PMC free article] [PubMed] [Google Scholar]
  2. Blanco M., Herrera G., Collado P., Rebollo J. E., Botella L. M. Influence of RecA protein on induced mutagenesis. Biochimie. 1982 Aug-Sep;64(8-9):633–636. doi: 10.1016/s0300-9084(82)80102-8. [DOI] [PubMed] [Google Scholar]
  3. Castellazzi M., George J., Buttin G. Prophage induction and cell division in E. coli. I. Further characterization of the thermosensitive mutation tif-1 whose expression mimics the effect of UV irradiation. Mol Gen Genet. 1972;119(2):139–152. doi: 10.1007/BF00269133. [DOI] [PubMed] [Google Scholar]
  4. Kogoma T., Torrey T. A., Connaughton M. J. Induction of UV-resistant DNA replication in Escherichia coli: induced stable DNA replication as an SOS function. Mol Gen Genet. 1979 Oct 2;176(1):1–9. doi: 10.1007/BF00334288. [DOI] [PubMed] [Google Scholar]
  5. Lark K. G., Lark C. A. recA-dependent DNA replication in the absence of protein synthesis: characteristics of a dominant lethal replication mutation, dnaT, and requirement for recA+ function. Cold Spring Harb Symp Quant Biol. 1979;43(Pt 1):537–549. doi: 10.1101/sqb.1979.043.01.059. [DOI] [PubMed] [Google Scholar]
  6. Little J. W., Mount D. W. The SOS regulatory system of Escherichia coli. Cell. 1982 May;29(1):11–22. doi: 10.1016/0092-8674(82)90085-x. [DOI] [PubMed] [Google Scholar]
  7. MAALOE O., HANAWALT P. C. Thymine deficiency and the normal DNA replication cycle. I. J Mol Biol. 1961 Apr;3:144–155. doi: 10.1016/s0022-2836(61)80041-7. [DOI] [PubMed] [Google Scholar]
  8. Miller J. H. Carcinogens induce targeted mutations in Escherichia coli. Cell. 1982 Nov;31(1):5–7. doi: 10.1016/0092-8674(82)90398-1. [DOI] [PubMed] [Google Scholar]
  9. Mount D. W. A mutant of Escherichia coli showing constitutive expression of the lysogenic induction and error-prone DNA repair pathways. Proc Natl Acad Sci U S A. 1977 Jan;74(1):300–304. doi: 10.1073/pnas.74.1.300. [DOI] [PMC free article] [PubMed] [Google Scholar]
  10. Walker G. C. Mutagenesis and inducible responses to deoxyribonucleic acid damage in Escherichia coli. Microbiol Rev. 1984 Mar;48(1):60–93. doi: 10.1128/mr.48.1.60-93.1984. [DOI] [PMC free article] [PubMed] [Google Scholar]
  11. Witkin E. M., McCall J. O., Volkert M. R., Wermundsen I. E. Constitutive expression of SOS functions and modulation of mutagenesis resulting from resolution of genetic instability at or near the recA locus of Escherichia coli. Mol Gen Genet. 1982;185(1):43–50. doi: 10.1007/BF00333788. [DOI] [PubMed] [Google Scholar]
  12. Witkin E. M. Thermal enhancement of ultraviolet mutability in a tif-1 uvrA derivative of Escherichia coli B-r: evidence that ultraviolet mutagenesis depends upon an inducible function. Proc Natl Acad Sci U S A. 1974 May;71(5):1930–1934. doi: 10.1073/pnas.71.5.1930. [DOI] [PMC free article] [PubMed] [Google Scholar]
  13. Witkin E. M. Ultraviolet mutagenesis and inducible DNA repair in Escherichia coli. Bacteriol Rev. 1976 Dec;40(4):869–907. doi: 10.1128/br.40.4.869-907.1976. [DOI] [PMC free article] [PubMed] [Google Scholar]
  14. Witkin E. M., Wermundsen I. E. Targeted and untargeted mutagenesis by various inducers of SOS functions in Escherichia coli. Cold Spring Harb Symp Quant Biol. 1979;43(Pt 2):881–886. doi: 10.1101/sqb.1979.043.01.095. [DOI] [PubMed] [Google Scholar]

Articles from Proceedings of the National Academy of Sciences of the United States of America are provided here courtesy of National Academy of Sciences

RESOURCES