SOS Response

Martine Defais, Pharmacology and Structural Biology Institute, Toulouse, France
Raymond Devoret, Curie Institute, Paris, France

Published online: September 2005

DOI: 10.1038/npg.els.0003874

Bacteria have developed an SOS response to mend DNA damage caused by deleterious agents such as radiations and chemicals. Mutagenesis, one of the SOS functions, has permitted bacteria to adapt to short- and long-term adverse living conditions.

Keywords: SOS signal; RecA nucleoprotein filament; SOS induction; LexA repressor; SOS mutagenesis

Figure 1. From DNA lesions to SOS functions. (1) Damage to DNA, (2) nature of SOS-inducing signal, (3) inactivation of repressors and mutagenesis proteins, (4) induced molecular reaction, (5) expressed SOS genes, and (6) SOS-induced functions. E, early; D, delayed.
Figure 2. Regulation of SOS genes. (a) In steady state, the replication fork proceeds normally. The SOS genes, four of which are represented with LexA repressor bound to their operator, express small amount of protein, except for the tightly repressed umuDC operon. (b) Following DNA damage and the appearance of SOS-inducing signals, early LexA cleavage occurs, catalysed by RecA nucleofilament on a blocked replication fork. SOS genes are expressed, among which are DNA repair genes. When mutagenesis proteins (UmuDC proteins) are produced, UmuD is processed in the presence of RecA nucleofilament, leading to mutagenesis. When DNA is repaired, SOS signals disappear and the cell reverts to steady state.
Figure 3. Induction of phage genes by cI repressor. (a) In the steady state, phage genes are repressed by phage cI repressor. (b) Following DNA damage and a blocked replication fork, RecA nucleofilament catalyses repressor cleavage, leading to phage production.
Figure 4. Time of gene expression during the cell cycle. Gene inducibility measured as the strength of LexA binding to the SOS operators–promoters is represented as the ordinate. In the abscissa, the operators–promoters of the SOS genes are aligned, following sequential induction during the cell cycle.
Figure 5. Molecular mechanism of SOS mutagenesis.
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 References
    Ames BN, Durson WE, Yamasaki E and Lee FD (1973) Carcinogens are mutagens: a single test combining liver homogenates for activation and bacteria for detection. Proceedings of the National Academy of Sciences of the USA 70: 2281–2285.
    Boudsocq F, Campbell M, Devoret R and Bailone A (1997) Quantitation of the inhibition of Hfr x F– recombination by the mutagenesis complex UmuD¢C. Journal of Molecular Biology 270: 201–211.
    Cayrol C, Petit C, Raynaud B et al. (1995) Recovery of respiration following the SOS response of Escherichia coli requires RecA-mediated induction of 2-keto-4-hydroxyglutarate aldolase. Proceedings of the National Academy of Sciences of the USA 92: 11806–11809.
    Eller MS, Maeda T, Magnoni C, Atwal D and Gilchrest BA (1997) Enhancement of DNA repair in human skin cells by thymidine dinucleotides: evidence for a p53-mediated mammalian SOS response. Proceedings of the National Academy of Sciences of the USA 94: 12627–12632.
    Fornace AJ (1992) Mammalian genes induced by radiation: activation of genes associated with growth control. Annual Review of Genetics 26: 507–526.
    George J, Devoret R and Radman M (1974) Indirect ultraviolet-reactivation of phage lambda. Proceedings of the National Academy of Sciences of the USA 71: 144–147.
    Heinemann B and Howard AJ (1965) Effect of compounds with both antitumor and bacteriophage-inducing activities on Escherichia coli nucleic acid synthesis. Antimicrobial Agents and Chemotherapy 5: 488–492.
    Howard-Flanders P and Boyce RP (1965) DNA repair and genetic recombination: studies on mutants of E. coli defective in these processes. Radiation Research 6(suppl.): 156–184.
    Kastan MB, Onyekwere O, Sidransky D, Vogelstein B and Craig RW (1991) Participation of p53 protein in the cellular response to DNA damage. Cancer Research 51: 6304–6311.
    Kenyon CJ and Walker GC (1980) DNA-damaging agents stimulate gene expression at specific loci in Escherichia coli. Proceedings of the National Academy of Sciences of the USA 77: 2819–2823.
    Lewis LK, Harlow GR, Gregg-Jolly LA and Mount DW (1994) Identification of high affinity binding sites for LexA which define new DNA damage-inducible genes in Escherichia coli. Journal of Molecular Biology 241: 507–523.
    Little JW and Mount DW (1982) The SOS regulatory system of E. coli. Cell 29: 11–22.
    book Radman M (1974) "Phenomenology of an inducible mutagenic DNA repair: SOS repair hypothesis". In: Prakasch L, Sherman F, Miller M, Lawrence C and Tabor HW (eds) Molecular and Environmental Aspects of Mutagenesis, pp. 128–142. Springfield IL: Thomas.
    Sassanfar M and Roberts JW (1990) Nature of the SOS inducing signal in E. coli: the involvement of DNA replication. Journal of Molecular Biology 212: 79–96.
    Schnarr M, Oertel-Buchheit P, Kazmaier M and Granger-Schnarr M (1991) DNA binding properties of the LexA repressor. Biochimie 73: 423–431.
    Sommer S, Bailone A and Devoret R (1993) The appearance of the UmuD¢C protein complex in Escherichia coli switches repair from homologous recombination to SOS mutagenesis. Molecular Microbiology 10: 963–971.
    Thompson LH and Schild D (2001) Homologous recombinational repair of DNA ensures mammalian chromosome stability. Mutation Research 477: 131–153.
    Valerie K, Delers A, Bruck C et al. (1988) Activation of human immunodeficiency virus type 1 by DNA damage in human cells. Nature 333: 78–81.
    Witkin EM (1976) Ultraviolet mutagenesis and inducible DNA repair in Escherichia coli. Bacteriological Reviews 40: 869–907.
 Further Reading
    Cox MM (1998) A broadening view of recombinational DNA repair in bacteria. Genes to Cells 3: 65–78.
    book Friedberg EC, Walker GC and Siede W (1995) DNA Repair and Mutagenesis Washington, DC: ASM Press.
    Kim B and Little JW (1992) Dimerization of a specific DNA-binding protein on the DNA. Science 255: 203–206.
    Kowalczykowski SC, Dixon DA, Eggelston AK, Lauder SD and Rehauer WM (1994) Biochemistry of homologous recombination in Escherichia coli. Microbiological Reviews 58: 401–465.
    Roca AI and Cox MM (1997) RecA protein: structure, function, and role in recombinational DNA repair. Progress in Nucleic Acids Research and Molecular Biology 56: 129–223.
    Sarasin A (1985) SOS response in mammalian cells. Cancer Investigation 3: 163–174.
    Sommer S, Boudsocq F, Devoret R and Bailone A (1998) Specific RecA amino acid changes affect RecA-UmuD¢C interaction. Molecular Microbiology 28: 281–291.
    Sutton MD, Smith BT, Godoy VG and Walker GC (2000) The SOS response: recent insights into umuDC-dependent mutagenesis and DNA damage tolerance. Annual Review of Genetics 34: 479–497.
    Vispé S and Defais M (1997) Mammalian Rad51 protein: a RecA homologue with pleiotropic functions. Biochimie 79: 587–592.
    Zhou BBS and Elledge SJ (2000) The DNA damage response: putting checkpoints in perspective. Nature 408: 433–439.

Related Sub-Topics:

DNA Damage and Repair | Biomolecular Interactions | Nucleic Acids: Structure, Function, Metabolism | Genomes and Chromosomes
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Article Title: SOS Response
 
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Defais, Martine, and Devoret, Raymond(Sep 2005) SOS Response. In: eLS. John Wiley & Sons Ltd, Chichester. http://www.els.net [doi: 10.1038/npg.els.0003874]