Programming stress-induced altruistic death in engineered bacteria.
Abstract
Programmed death is often associated with a bacterial stress response. This behavior
appears paradoxical, as it offers no benefit to the individual. This paradox can be
explained if the death is 'altruistic': the killing of some cells can benefit the
survivors through release of 'public goods'. However, the conditions where bacterial
programmed death becomes advantageous have not been unambiguously demonstrated experimentally.
Here, we determined such conditions by engineering tunable, stress-induced altruistic
death in the bacterium Escherichia coli. Using a mathematical model, we predicted
the existence of an optimal programmed death rate that maximizes population growth
under stress. We further predicted that altruistic death could generate the 'Eagle
effect', a counter-intuitive phenomenon where bacteria appear to grow better when
treated with higher antibiotic concentrations. In support of these modeling insights,
we experimentally demonstrated both the optimality in programmed death rate and the
Eagle effect using our engineered system. Our findings fill a critical conceptual
gap in the analysis of the evolution of bacterial programmed death, and have implications
for a design of antibiotic treatment.
Type
Journal articleSubject
ApoptosisEscherichia coli
Genetic Engineering
Microbial Viability
Models, Biological
Reproducibility of Results
Stress, Physiological
Permalink
https://hdl.handle.net/10161/9352Published Version (Please cite this version)
10.1038/msb.2012.57Publication Info
Tanouchi, Yu; Pai, Anand; Buchler, Nicolas E; & You, Lingchong (2012). Programming stress-induced altruistic death in engineered bacteria. Mol Syst Biol, 8. pp. 626. 10.1038/msb.2012.57. Retrieved from https://hdl.handle.net/10161/9352.This is constructed from limited available data and may be imprecise. To cite this
article, please review & use the official citation provided by the journal.
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Show full item recordScholars@Duke
Nicolas Buchler
Assistant Professor of Biology
Our lab is interested in the systems biology and evolution of epigenetic switches
(bistability) and clocks (oscillators) in gene regulatory networks, two functions
that are essential for patterning, cell proliferation, and differentiation in biological
systems. We also study biochemical oscillators such as the cell cycle, metabolic rhythms,
and circadian clocks, which co-exist in the same cells and interact with one another
through shared resources.
Lingchong You
Professor of Biomedical Engineering
The You lab uses a combination of mathematical modeling, machine learning, and quantitative
experiments to elucidate principles underlying the dynamics of microbial communities
in time and space and to control these dynamics for applications in computation, engineering,
and medicine.
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