期刊
CURRENT GENETICS
卷 67, 期 2, 页码 295-303出版社
SPRINGER
DOI: 10.1007/s00294-020-01134-3
关键词
DNA polymerase IV; Regulator; Single-molecule live-cell imaging; SOS response
资金
- Australian Research Council [FL140100027]
- National Health and Medical Research Council [APP1165135]
- Australian Research Council [FL140100027] Funding Source: Australian Research Council
The study demonstrates that the formation of pol IV foci in E. coli cells with DNA damage is recB-dependent, and UmuD and UmuDMODIFIER LETTER PRIME play important roles in modulating pol IV activity.
DNA polymerase IV (pol IV) is expressed at increased levels in Escherichia coli cells that suffer DNA damage. In a recent live-cell single-molecule fluorescence microscopy study, we demonstrated that the formation of pol IV foci is strongly recB-dependent in cells treated with the DNA break-inducing antibiotic ciprofloxacin. The results of that study support a model in which pol IV acts to extend D-loop structures during recombinational repair of DNA double-strand breaks. In the present study, we extend upon this work, investigating the UmuD and UmuDMODIFIER LETTER PRIME proteins as potential modulators of pol IV activity in ciprofloxacin-treated cells. We found that the non-cleavable mutant UmuD(K97A) promotes long-lived association of pol IV with the nucleoid, whereas its cleaved form, UmuDMODIFIER LETTER PRIME, which accumulates in DNA-damaged cells, reduces binding. The results provide additional support for a model in which UmuD and UmuDMODIFIER LETTER PRIME directly modulate pol IV-binding to the nucleoid.
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