Stressor interaction networks suggest antibiotic resistance co-opted from stress responses to temperature
Stressor interaction networks suggest antibiotic resistance co-opted from stress responses to temperature
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DOI：
10.1038/s41396-018-0241-7
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发表时间：
2019-01-01
期刊：
影响因子：
11
通讯作者：
Yeh, Pamela J.
中科院分区：
文献类型：
--
作者：
Cruz-Loya, Mauricio;Kang, Tina Manzhu;Yeh, Pamela J.
温度、压力和酸碱度等环境因素在一定程度上影响了生命的进化。随着生活的进步，新的应激源(如毒药和抗生素)作为有机体之间军备竞赛的一部分出现。在这里，我们问细胞是否利用了现有的机制来对新的应激源做出反应，或者是否新的反应是从头进化的。我们使用一种纯粹基于表型增长测量和应激源对人口增长影响之间的交互作用的网络聚类方法。我们将这种方法应用于两种类型的应激源--温度和抗生素--以发现它们在大肠杆菌中的细胞反应重叠的程度。我们的分类表明，对低温和高温的反应是明显分开的，每一种反应都与分别对冷或热有类似影响的抗生素的反应分在一起。作为进一步的支持，我们使用转录荧光报告文库来证实热休克和冷休克基因是由抗生素诱导的。我们还表明，在高温下进化的菌株对模拟寒冷影响的抗生素更敏感。综上所述，我们的结果强烈表明，温度应激反应已被用于应对抗生素应激。
Environmental factors like temperature, pressure, and pH partly shaped the evolution of life. As life progressed, new stressors (e.g., poisons and antibiotics) arose as part of an arms race among organisms. Here we ask if cells co-opted existing mechanisms to respond to new stressors, or whether new responses evolved de novo. We use a network-clustering approach based purely on phenotypic growth measurements and interactions among the effects of stressors on population growth. We apply this method to two types of stressors-temperature and antibiotics-to discover the extent to which their cellular responses overlap in Escherichia coli. Our clustering reveals that responses to low and high temperatures are clearly separated, and each is grouped with responses to antibiotics that have similar effects to cold or heat, respectively. As further support, we use a library of transcriptional fluorescent reporters to confirm heat-shock and cold-shock genes are induced by antibiotics. We also show strains evolved at high temperatures are more sensitive to antibiotics that mimic the effects of cold. Taken together, our results strongly suggest that temperature stress responses have been co-opted to deal with antibiotic stress.