SOS Response

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General Description

A set of reversible checkpoints induced upon DNA damage, or regions of single stranded DNA.

Components

Function

Repair DNA damage

Regulation

RecA bound to single-stranded DNA leads to its activation. This activated form of RecA, or RecA* causes autocleavage of the LexA repressor[1]. It was later discovered that the mechanism of LexA cleavage is autodigestion catalyzed by RecA*[2].

Cell Biology

The expression of multiple genes is upregulated upon induction of the SOS response. The LexA repressor control the expression of:

  • sulA[3]
  • ftsK[4]
  • uvrA[5]
  • uvrB[6]
  • Peterson et al. (1988) finds that the derepression of other specific genes promote DNA repair and mutagenesis[7].

Experimental Resources

Several antibiotics induce the SOS response

  • mitomycin C (working concentration-0.1 µg/ml)[4]

Comparison with other organisms

Notes

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References

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  1. ↑ Little, JW () Control of the SOS regulatory system by the level of RecA protease. Biochimie 64 585-9 PubMed
  2. ↑ Little, JW (1984) Autodigestion of lexA and phage lambda repressors. Proc. Natl. Acad. Sci. U.S.A. 81 1375-9 PubMed
  3. ↑ Mizusawa, S et al. (1983) Transcription of the sulA gene and repression by LexA. J. Mol. Biol. 171 337-43 PubMed
  4. ↑ 4.0 4.1 Wang, L & Lutkenhaus, J (1998) FtsK is an essential cell division protein that is localized to the septum and induced as part of the SOS response. Mol. Microbiol. 29 731-40 PubMed
  5. ↑ Sancar, A et al. (1982) LexA protein inhibits transcription of the E. coli uvrA gene in vitro. Nature 298 96-8 PubMed
  6. ↑ Sancar, GB et al. (1982) The uvrB gene of Escherichia coli has both lexA-repressed and lexA-independent promoters. Cell 28 523-30 PubMed
  7. ↑ Peterson, KR et al. (1988) Derepression of specific genes promotes DNA repair and mutagenesis in Escherichia coli. J. Bacteriol. 170 1-4 PubMed