The role of Acinetobacter baumannii ATCC 17978 UmuDC homologs A1S-0636-A1S-0637, A1S-1174-A1S-1173, and A1S-1389 (UmuDAb) 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 umuDAb 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 umuDAb 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. Copyright © 2014, American Society for Microbiology. All Rights Reserved.
CITATION STYLE
Aranda, J., López, M., Leiva, E., Magán, A., Adler, B., Bou, G., & Barbé, J. (2014). Role of Acinetobacter baumannii UmuD homologs in antibiotic resistance acquired through DNA damage-induced mutagenesis. Antimicrobial Agents and Chemotherapy, 58(3), 1771–1773. https://doi.org/10.1128/AAC.02346-13
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