Escherichia coli cells defective for the recN gene display constitutive elevation of mutagenesis at 3,N4-ethenocytosine via an SOS-induced mechanism
Article first published online: 18 JAN 2002
Volume 37, Issue 3, pages 680–686, August 2000
How to Cite
Dunman, P. M., Ren, L., Rahman, M. S., Palejwala, V. A., Murphy, H. S., Volkert, M. R. and Humayun, M. Z. (2000), Escherichia coli cells defective for the recN gene display constitutive elevation of mutagenesis at 3,N4-ethenocytosine via an SOS-induced mechanism. Molecular Microbiology, 37: 680–686. doi: 10.1046/j.1365-2958.2000.02045.x
- Issue published online: 18 JAN 2002
- Article first published online: 18 JAN 2002
- Accepted 31 May, 2000.
The Escherichia coli UVM (UV Modulation of mutagenesis) response is a DNA damage-inducible mutagenic pathway detected as significantly increased mutagenesis at 3,N4-ethenocytosine (εC) lesions borne on transfected single-stranded M13 vector DNA. All major classes of DNA-damaging agents can induce UVM, and the phenomenon is independent of previously characterized mutagenic responses in E. coli. To understand this phenomenon further, we set out to identify and characterize mutants in the UVM response. Screening a mutant bank of cells defective for 1-methyl-3-nitro-1-nitrosoguanidine-inducible genes revealed that defects in the recN gene cause a constitutive elevation of mutagenesis at εC residues. In contrast to normal cells that show ≈ 6% mutagenesis at εC lesions, but ≈ 60% upon UVM induction, recN-defective strains display approximately 50% mutagenesis at εC lesion sites in untreated cells. However, the recN-mediated mutagenesis response was found to require the recA gene and the umuDC genes, and could be suppressed in the presence of a plasmid harbouring the SOS transcriptional repressor LexA. These results imply that recN cells are constitutively active for SOS mutagenesis functions. The observation that εC mutagenesis is enhanced in recN cells confirms previous findings that mutagenesis at εC can also be independently elevated by the SOS pathway.