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Errors in mutagenesis and the benefit of cell-to-cell signalling in the evolution of stress-induced mutagenesis.

ABSTRACT: Stress-induced mutagenesis is a widely observed phenomenon. Theoretical models have shown that stress-induced mutagenesis can be favoured by natural selection due to the beneficial mutations it generates. These models, however, assumed an error-free regulation of mutation rate in response to stress. Here, we explore the effects of errors in the regulation of mutagenesis on the evolution of stress-induced mutagenesis, and consider the role of cell-to-cell signalling. Using theoretical models, we show (i) that stress-induced mutagenesis can be disadvantageous if errors are common; and (ii) that cell-to-cell signalling can allow stress-induced mutagenesis to be favoured by selection even when error rates are high. We conclude that cell-to-cell signalling can facilitate the evolution of stress-induced mutagenesis in microbes through second-order selection.

SUBMITTER: Dellus-Gur E

PROVIDER: S-EPMC5717628 | biostudies-literature | 2017 Nov

REPOSITORIES: biostudies-literature

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Errors in mutagenesis and the benefit of cell-to-cell signalling in the evolution of stress-induced mutagenesis.

Dellus-Gur Eynat E Ram Yoav Y Hadany Lilach L

Royal Society open science 20171101 11

Stress-induced mutagenesis is a widely observed phenomenon. Theoretical models have shown that stress-induced mutagenesis can be favoured by natural selection due to the beneficial mutations it generates. These models, however, assumed an error-free regulation of mutation rate in response to stress. Here, we explore the effects of errors in the regulation of mutagenesis on the evolution of stress-induced mutagenesis, and consider the role of cell-to-cell signalling. Using theoretical models, we ...[more]

PMID: 29291054

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Project description:BACKGROUND: Microbial tolerance to different environmental stresses is of importance for efficient production of biofuels and biochemical. Such traits are often improved by evolutionary engineering approaches including mutagen-induced mutagenesis and successive passage. In contrast to these approaches which generate mutations in rapidly growing cells, recent research showed that mutations could be generated in non-dividing cells under stressful but non-lethal conditions, leading to the birth of the theory of stress-induced mutagenesis (SIM). A molecular mechanism of SIM has been elucidated to be mutagenic repair of DNA breaks. This inspired us to develop a synthetic SIM module to simulate the mutagenic cellular response so as to accelerate microbial adaptive evolution for an improved stress tolerance. RESULTS: A controllable SIM evolution module was devised based on a genetic toggle switch in Escherichia coli. The synthetic module enables expression and repression of the genes related to up- and down-regulation responses during SIM in a bistable way. Upon addition of different inducers, the module can be turned on or off, triggering transition to a mutagenic or a high-fidelity state and thus allowing periodic adaptive evolution. Six genes (recA, dinB, umuD, ropS, ropE, and nusA) in the up-regulation responses were evaluated for their potentials to enhance the SIM rate. Expression of recA, dinB, or ropS alone increased the SIM rate by 4.5- to 13.7-fold, whereas their combined expression improved the rate by 31.9-fold. Besides, deletion of mutL increased the SIM rate by 82-fold. Assembly of these genes into the SIM module in the mutL-deletion E. coli strain elevated the SIM rate by nearly 3000-fold. Accelerated adaptive evolution of E. coli equipped with this synthetic SIM module was demonstrated under n-butanol stress, with the minimal inhibitory concentration of n-butanol increasing by 56 % within 2.5 months. CONCLUSIONS: A synthetic SIM module was constructed to simulate cellular mutagenic responses during SIM. Based on this, a novel evolutionary engineering approach-SIM-based adaptive evolution-was developed to improve the n-butanol tolerance of E. coli.

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Errors in mutagenesis and the benefit of cell-to-cell signalling in the evolution of stress-induced mutagenesis.

Publications

Errors in mutagenesis and the benefit of cell-to-cell signalling in the evolution of stress-induced mutagenesis.

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