期刊
ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
卷 58, 期 3, 页码 1771-1773出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/AAC.02346-13
关键词
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资金
- Ministerio de Ciencia e Innovacion [BFU2011-23478]
- European Community [278232]
- Ministerio de Ciencia e Innovacion, Instituto de Salud Carlos III
- Spanish Network for Research in Infectious Diseases [REIPI RD12/0015]
- FIS [PI12/00552]
- Instituto de Salud Carlos III (Madrid, Spain)
The role of Acinetobacter baumannii ATCC 17978 UmuDC homologs A1S_0636-A1S_0637, A1S_1174-A1S_1173, and A1S_1389 (UmuD(Ab)) in antibiotic resistance acquired through UV-induced mutagenesis was evaluated. Neither the growth rate nor the UV-related survival of any of the three mutants was significantly different from that of the wild-type parental strain. However, all mutants, and especially the umuD(Ab) mutant, were less able to acquire resistance to rifampin and streptomycin through the activities of their error-prone DNA polymerases. Furthermore, in the A. baumannii mutant defective in the umuD(Ab) gene, the spectrum of mutations included a dramatic reduction in the frequency of transition mutations, the mutagenic signature of the DNA polymerase V encoded by umuDC.
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