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.
|Journal||Antimicrobial Agents and Chemotherapy|
|Publication status||Published - 1 Mar 2014|