|
ИСТИНА |
Войти в систему Регистрация |
Интеллектуальная Система Тематического Исследования НАукометрических данных |
||
Bioinformatics Analysis of Genes of Streptomyces Xinghaiensis (Fradiae) ATCC 19609 With a Focus on Mutations Conferring Resistance to Oligomycin A and Its Derivativesстатья
Информация о цитировании статьи получена из
Web of Science
Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 25 ноября 2020 г.
- Авторы: Vatlin AA, Bekker OB, Lysenkova LN, Shchekotikhin AE, Danilenko VN
- Журнал: JOURNAL OF GLOBAL ANTIMICROBIAL RESISTANCE
- Том: 22
- Номер: 47
- Год издания: 2020
- Первая страница: 47
- Последняя страница: 53
- DOI: 10.1016/j.jgar.2020.01.026.
- Аннотация: Objectives: The aim of this study was to obtain Streptomyces xinghaiensis (fradiae) ATCC 19609 mutants resistant to oligomycin A and its derivatives and to identify the underlying mechanism of resistance. This study was based on the premise that S. xinghaiensis ATCC 19609 contains several oligomycin A biological targets, explaining why the strain remains supersensitive to oligomycin A despite all efforts to obtain resistant mutants using standard genetic methods.Methods: The method to obtain oligomycin A-resistant mutants was performed in two steps: first, mutants slightly resistant to an oligomycin A derivative with an attenuated effect were obtained; and second, oligomycin A-resistant mutants were obtained from those mutants obtained earlier. The genomes of the mutants were then sequenced and a bioinformatics analysis of the detected mutations was conducted.Results: Mutants with seven mutations were required to obtain oligomycin A-resistant mutant strains of S. xinghaiensis characterised by a level of resistance comparable with that of the model organism Streptomyces lividans. Five of these mutations caused amino acid substitutions in the well-known oligomycin A biological target, namely the F0F1-ATP synthase A subunit, and the others caused amino acid substitutions in unexplored biological targets, including RecB-like recombinase, type IV helicase, DNA ligase and single-domain response regulator.Conclusion: A new oligomycin resistance mechanism involving a pathway that repairs double-strand breaks in DNA known as non-homologous end joining (NHEJ) was discovered.
- Добавил в систему: Щекотихин Андрей Егорович