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
To postpone Septation until DNA is repaired.
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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- ↑ Little, JW () Control of the SOS regulatory system by the level of RecA protease. Biochimie 64 585-9 PubMed
- ↑ Little, JW (1984) Autodigestion of lexA and phage lambda repressors. Proc. Natl. Acad. Sci. U.S.A. 81 1375-9 PubMed
- ↑ Mizusawa, S et al. (1983) Transcription of the sulA gene and repression by LexA. J. Mol. Biol. 171 337-43 PubMed
- ↑ 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
- ↑ Sancar, A et al. (1982) LexA protein inhibits transcription of the E. coli uvrA gene in vitro. Nature 298 96-8 PubMed
- ↑ Sancar, GB et al. (1982) The uvrB gene of Escherichia coli has both lexA-repressed and lexA-independent promoters. Cell 28 523-30 PubMed
- ↑ Peterson, KR et al. (1988) Derepression of specific genes promotes DNA repair and mutagenesis in Escherichia coli. J. Bacteriol. 170 1-4 PubMed