PMID:12791149
| Citation |
Bradshaw, JS and Kuzminov, A (2003) RdgB acts to avoid chromosome fragmentation in Escherichia coli. Mol. Microbiol. 48:1711-25 |
|---|---|
| Abstract |
Bacterial RecA protein is required for repair of two-strand DNA lesions that disable whole chromosomes. recA mutants are viable, suggesting a considerable cellular capacity to avoid these chromosome-disabling lesions. recA-dependent mutants reveal chromosomal lesion avoidance pathways. Here we characterize one such mutant, rdgB/yggV, deficient in a putative inosine/xanthosine triphosphatase, conserved throughout kingdoms of life. The rdgB recA lethality is suppressed by inactivation of endonuclease V (gpnfi) specific for DNA-hypoxanthines/xanthines, suggesting that RdgB either intercepts improper DNA precursors dITP/dXTP or works downstream of EndoV in excision repair of incorporated hypoxathines/xanthines. We find that DNA isolated from rdgB mutants contains EndoV-recognizable modifications, whereas DNA from nfi mutants does not, substantiating the dITP/dXTP interception by RdgB. rdgB recBC cells are inviable, whereas rdgB recF cells are healthy, suggesting that chromosomes in rdgB mutants suffer double-strand breaks. Chromosomal fragmentation is indeed observed in rdgB recBC mutants and is suppressed in rdgB recBC nfi mutants. Thus, one way to avoid chromosomal lesions is to prevent hypoxanthine/xanthine incorporation into DNA via interception of dITP/dXTP. |
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| Keywords |
Chromosomes, Bacterial/genetics; DNA Damage; DNA Repair; Deoxyribonuclease (Pyrimidine Dimer); Endodeoxyribonucleases/genetics; Endodeoxyribonucleases/metabolism; Escherichia coli/genetics; Escherichia coli/growth & development; Escherichia coli/metabolism; Escherichia coli Proteins/genetics; Escherichia coli Proteins/metabolism; Exodeoxyribonuclease V; Exodeoxyribonucleases/genetics; Exodeoxyribonucleases/metabolism; Mutagenesis, Insertional; Mutation; Plasmids/genetics; Pyrophosphatases/genetics; Pyrophosphatases/metabolism |
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