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Escherichia coli cells defective for the recN gene display constitutive elevation of mutagenesis at 3,N 4 ‐ethenocytosine via an SOS‐induced mechanism
Author(s) -
Dunman Paul M.,
Ren Li,
Rahman M. Sayeedur,
Palejwala Vaseem A.,
Murphy Holly S.,
Volkert Michael R.,
Humayun M. Zafri
Publication year - 2000
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1046/j.1365-2958.2000.02045.x
Subject(s) - biology , mutagenesis , escherichia coli , mechanism (biology) , gene , genetics , sos response , computational biology , mutation , microbiology and biotechnology , philosophy , epistemology
The Escherichia coli UVM ( UV M odulation of mutagenesis) response is a DNA damage‐inducible mutagenic pathway detected as significantly increased mutagenesis at 3,N 4 ‐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.