Author:
Aranda Jesús,López Mario,Leiva Enoy,Magán Andrés,Adler Ben,Bou Germán,Barbé Jordi
Abstract
ABSTRACTThe role ofAcinetobacter baumanniiATCC 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 theumuDAbmutant, were less able to acquire resistance to rifampin and streptomycin through the activities of their error-prone DNA polymerases. Furthermore, in theA. baumanniimutant defective in theumuDAbgene, the spectrum of mutations included a dramatic reduction in the frequency of transition mutations, the mutagenic signature of the DNA polymerase V encoded byumuDC.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Pharmacology (medical),Pharmacology
Cited by
21 articles.
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