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Comment
. 2005 Jul;3(7):e255.
doi: 10.1371/journal.pbio.0030255. Epub 2005 Jul 12.

After 30 years of study, the bacterial SOS response still surprises us

Bénédicte Michel  1
Affiliations
Comment

After 30 years of study, the bacterial SOS response still surprises us

Bénédicte Michel. PLoS Biol. 2005 Jul.

Abstract

The bacterial SOS response kicks in when bacteria experience DNA damage, and helps the organisms correct and survive DNA damage events. This primer provides a foundation for understanding these events.

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Figures

Figure 1
Figure 1. An Oscillatory Behavior for the SOS Response
In non-induced growth conditions, the LexA repressor binds to SOS-controlled promoters, limiting or preventing their action. The basal level of expression of the genes that belong to the SOS regulon is variable. For example, in non-induced cells there are 7,500 molecules of RecA and undetectable amounts of Pol V. Upon DNA damage, RecA filaments formed at sites of damage activate the autocleavage of the LexA repressor, allowing SOS gene expression. SOS induction is reversed when damages are repaired. This is due to the disappearance of the RecA filament and allows the newly synthesized LexA molecules to bind SOS promoters. The recent work by Joel Stavans' laboratory provides evidence that, after DNA damage, individual cells oscillate between an induced and a less-induced state, and that the level of DNA damage governs the number of high-induced phases rather than their amplitude and timing [11]. Grey circles, LexA; white circles, RecA.
Figure 2
Figure 2. A Model for SOS-Dependent Evolution to Antibiotic Resistance
Topoisomerase poisoning agents cause DNA double-strand breaks. RecBC in turn loads RecA. RecA filaments induce the SOS response and recombine. The homologous recombination reaction ends with a primer-template structure to which SOS-induced polymerases have access. DNA synthesis by these low-fidelity polymerases is accompanied by the introduction of mutations. A sub-population of mutant cells that can resist the poisoning agent invade the niche. The break-induced erroneous repair model, originally proposed for the mutagenic effects of DNA double-strand breaks in various laboratory conditions, accounts for the emergence of ciprofloxacin-resistant bacteria in a murine infection model [18]. Indented circles, RecBC; stars, SOS-induced DNA polymerases; triangle, mutation; white circles, RecA.
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References

    1. Radman M. SOS repair hypothesis: Phenomenology of an inducible DNA repair which is accompanied by mutagenesis. Basic Life Sci. 1975;5A:355–367. - PubMed
    1. Kuzminov A. Recombinational repair of DNA damage in Escherichia coli and bacteriophage lambda. Microbiol Mol Biol Rev. 1999;63:751–813. - PMC - PubMed
    1. McPartland A, Green L, Echols H. Control of recA gene RNA in E. coli: Regulatory and signal genes. Cell. 1980;20:731–737. - PubMed
    1. Fernandez De Henestrosa AR, Ogi T, Aoyagi S, Chafin D, Hayes JJ, et al. Identification of additional genes belonging to the LexA regulon in Escherichia coli . Mol Microbiol. 2000;35:1560–1572. - PubMed
    1. Courcelle J, Khodursky A, Peter B, Brown PO, Hanawalt PC. Comparative gene expression profiles following UV exposure in wild- type and SOS-deficient Escherichia coli . Genetics. 2001;158:41–64. - PMC - PubMed

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