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首页> 外文期刊>The Journal of Antibiotics: An International Journal >Antibiotic resistance mutations induced in growing cells of Bacillus-related thermophiles
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Antibiotic resistance mutations induced in growing cells of Bacillus-related thermophiles

机译：芽孢杆菌相关嗜热嗜热植物生长细胞中诱导的抗生素抗性突变

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摘要

Stress-induced mutagenesis can assist pathogens in generating drug-resistant cells during antibiotic therapy; however, if and how antibiotics induce mutagenesis in microbes remains poorly understood. A non-pathogenic thermophile, Geobacillus kaustophilus HTA426, efficiently produces derivative cells resistant to rifampicin and streptomycin via rpoB and rpsL mutations, respectively. Here, we examined this phenomenon to suggest a novel mutagenic mode induced by antibiotics. Fluctuation analysis indicated that mutations occurred via spontaneous mutations during culture. However, mutations were much more frequent in growing cells than stationary cells, and mutation sites were varied through cell growth. These observations suggested that growing cells induced mutagenesis in response to antibiotics. An in-frame deletion of mfd, which governs transcription-coupled repair to correct DNA lesions on the transcribed strand, caused mutations that were comparable between growing and stationary cells; therefore, the mutagenic mechanism was attributable to DNA repair defects where growing cells depressed mfd function. Mutations occurred more frequently at optimal growth temperatures for G. kaustophilus than at a higher growth temperature, suggesting that the mutagenesis relies on active cellular activities rather than high temperature-associated DNA damage. In addition, the mutagenesis may involve a mutagenic factor targeting these sites, in addition to mfd depression, because rpoB and rpsL mutations were dominant at thymine and guanine sites on the transcribed strand. A similar mutagenic profile was observed for other Geobacillus and thermophilic Bacillus species. This suggests that Bacillus-related thermophiles commonly induce mutagenesis in response to rifampicin and streptomycin to produce resistant cells.
机译：应激诱导突变可以帮助病原体在抗生素治疗期间产生耐药细胞；然而，抗生素是否以及如何在微生物中诱发突变仍知之甚少。非致病性嗜热菌kaustophilus Geobillus HTA426通过rpoB和rpsL突变分别高效产生对利福平和链霉素耐药的衍生细胞。在这里，我们研究了这一现象，以提出一种由抗生素诱导的新型诱变模式。波动分析表明，突变是通过培养过程中的自发突变发生的。然而，在生长的细胞中，突变比在静止的细胞中要频繁得多，并且突变位点在细胞生长过程中会发生变化。这些观察结果表明，生长中的细胞会诱发抗生素引起的突变。mfd的框内缺失控制转录偶联修复，以纠正转录链上的DNA损伤，导致生长细胞和静止细胞之间的突变具有可比性；因此，突变机制可归因于DNA修复缺陷，即生长细胞抑制mfd功能。与更高的生长温度相比，在最佳生长温度下发生突变的频率更高，这表明突变依赖于活跃的细胞活动，而不是高温相关的DNA损伤。此外，除了mfd抑制外，突变可能还涉及针对这些位点的突变因子，因为rpoB和rpsL突变在转录链上的胸腺嘧啶和鸟嘌呤位点占优势。在其他土杆菌和嗜热杆菌物种中也观察到类似的诱变特征。这表明，与芽孢杆菌相关的嗜热菌通常会诱发对利福平和链霉素的诱变反应，从而产生耐药细胞。

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