Stressor interaction networks suggest antibiotic resistance co-opted from stress responses to temperature

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...

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Bibliographic Details
Published in:The ISME Journal 2019-01, Vol.13 (1), p.12-23
Main Authors: Cruz-Loya, Mauricio, Kang, Tina Manzhu, Lozano, Natalie Ann, Watanabe, Rina, Tekin, Elif, Damoiseaux, Robert, Savage, Van M., Yeh, Pamela J.
Format: Article
Language:English
Subjects:
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631/326/22/1290
Anti-Bacterial Agents - pharmacology
Antibiotic resistance
Antibiotics
Biological Evolution
Biomedical and Life Sciences
Clustering
Cold
Cold shock
Drug Resistance, Bacterial
E coli
Ecology
Environmental factors
Escherichia coli - drug effects
Escherichia coli - genetics
Escherichia coli - physiology
Evolutionary Biology
Fluorescence
Gene Library
High temperature
Life Sciences
Low temperature
Microbial Ecology
Microbial Genetics and Genomics
Microbiology
Poisons
Population growth
Stress, Physiological
Temperature
Temperature effects
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Summary: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.
ISSN:1751-7362
1751-7370
DOI:10.1038/s41396-018-0241-7