细菌慈善工作导致了全人口的抗药性
Henry H Lee1, Michael N Molla, Charles R Cantor
1Howard Hughes Medical Institute, Center for BioDynamics, Boston, Massachusetts 02115, USA.
Nature
|September 3, 2010
概括
高度耐药的细菌突变通过产生印,一个信号分子来保护脆弱的细胞. 这种"细菌利他主义"通过亲属选择提高了对抗生素的生存率.
科学领域:
- 微生物学 微生物学
- 进化生物学 进化生物学
- 遗传学 是一个遗传学.
背景情况:
- 细菌通过耐药机制表现出适应抗生素的能力.
- 发展抗生素耐药性的人口动态尚不清楚.
- 已知个体抗性等位基因和应激反应,但人口层面的策略不太清楚.
研究的目的:
- 在大肠杆菌 (Escherichia coli) 抗生素耐药性发展期间调查种群动态.
- 了解耐药突变物影响不那么耐药细胞生存的机制.
- 探索细菌信号分子在人口水平抗生素耐药性的作用.
主要方法:
- 持续培养大肠杆菌暴露于增加的抗生素水平.
- 与整个人群相比,对隔离物耐药性的分析.
- 转录简介用于识别分子机制.
- 耐药突变的全基因组测序. 耐药突变的全基因组测序.
主要成果:
- 大多数细菌分离的耐药性低于总人口.
- 高度耐药的突变物通过印生产提高了不太耐药细胞的生存率.
- 印多尔激活了药物排放和氧化应激防御系统.
- 抵抗突变是独立于英多尔生产的,这表明利他主义的健身成本.
结论:
- 确定了一种基于人口的抵抗机制,类似于亲属选择.
- 耐药突变物可以以适应性成本为脆弱细胞提供保护.
- 这种利他主义行为提高了在抗生素压力环境中的细菌总体存活率.
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