Sanders Laurie H, Sudhakaran Julee, Sutton Mark D
Department of Biochemistry, School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14214, USA.
FEMS Microbiol Lett. 2009 May;294(1):89-96. doi: 10.1111/j.1574-6968.2009.01550.x. Epub 2009 Mar 10.
Inactivation of the Pseudomonas aeruginosa mutM, mutY, or mutT gene conferred a 2.4-, 17.2-, or 38.1-fold increase in spontaneous mutation frequency, respectively. Importantly, the mutY and mutT strains each displayed a robust H(2)O(2)-induced mutation frequency. In addition, the mutM, mutY, and mutT mutations severely sensitized P. aeruginosa to killing by H(2)O(2), suggesting that these gene products act to repair one or more cytotoxic lesions in P. aeruginosa. Nucleotide sequence analysis of a fragment of the rpoB gene from rifampicin resistant mutM-, mutY-, and, mutT-deficient strains was consistent with this conclusion. These findings are discussed in terms of possible roles for mutM, mutY, and mutT in contributing to survival and mutagenesis of P. aeruginosa colonizing the airways of cystic fibrosis patients.
铜绿假单胞菌mutM、mutY或mutT基因的失活分别使自发突变频率增加了2.4倍、17.2倍或38.1倍。重要的是,mutY和mutT菌株各自表现出强烈的H₂O₂诱导的突变频率。此外,mutM、mutY和mutT突变使铜绿假单胞菌对H₂O₂杀伤极度敏感,这表明这些基因产物的作用是修复铜绿假单胞菌中的一种或多种细胞毒性损伤。来自耐利福平的mutM、mutY和mutT缺陷菌株的rpoB基因片段的核苷酸序列分析与这一结论一致。本文从mutM、mutY和mutT在囊性纤维化患者气道定植的铜绿假单胞菌的存活和诱变中的可能作用方面对这些发现进行了讨论。