The Bacillus Subtilis K-State Promotes Stationary-Phase Mutagenesis via Oxidative Damage.

Holly A Martin,Amanda A Kidman,Eduardo A Robleto,Carmen Vallin,Mario Pedraza-Reyes,Jillian Socea

doi:10.3390/genes11020190

Holly A Martin, Amanda A Kidman + Show 4 more

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https://doi.org/10.3390/genes11020190

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Abstract

Bacterial cells develop mutations in the absence of cellular division through a process known as stationary-phase or stress-induced mutagenesis. This phenomenon has been studied in a few bacterial models, including Escherichia coli and Bacillus subtilis; however, the underlying mechanisms between these systems differ. For instance, RecA is not required for stationary-phase mutagenesis in B. subtilis like it is in E. coli. In B. subtilis, RecA is essential to the process of genetic transformation in the subpopulation of cells that become naturally competent in conditions of stress. Interestingly, the transcriptional regulator ComK, which controls the development of competence, does influence the accumulation of mutations in stationary phase in B. subtilis. Since recombination is not involved in this process even though ComK is, we investigated if the development of a subpopulation (K-cells) could be involved in stationary-phase mutagenesis. Using genetic knockout strains and a point-mutation reversion system, we investigated the effects of ComK, ComEA (a protein involved in DNA transport during transformation), and oxidative damage on stationary-phase mutagenesis. We found that stationary-phase revertants were more likely to have undergone the development of competence than the background of non-revertant cells, mutations accumulated independently of DNA uptake, and the presence of exogenous oxidants potentiated mutagenesis in K-cells. Therefore, the development of the K-state creates conditions favorable to an increase in the genetic diversity of the population not only through exogenous DNA uptake but also through stationary-phase mutagenesis.

Highlights

For over 60 years, genetic experiments have shown that bacterial cells can develop mutations in the absence of growth; this is known as stationary-phase mutagenesis or stress-induced mutagenesis [1,2,3].This type of mutagenic processes is independent of growth, and is observed in bacteria and eukaryotes.they expand our view of the evolutionary process and can explain the formation of mutations that confer antibiotic resistance and cancers [1]
We examined the idea that the development of the K-state leads to conditions that predispose cells to accumulate stationary-phase mutations even in the absence of DNA uptake that provides the substrate for genetic recombination
ComK factors which control the development of competence, a state in which cells incorporate foreign DNA into the chromosome via homologous recombination [2]

Summary

Introduction

For over 60 years, genetic experiments have shown that bacterial cells can develop mutations in the absence of growth; this is known as stationary-phase mutagenesis or stress-induced mutagenesis [1,2,3].This type of mutagenic processes is independent of growth, and is observed in bacteria and eukaryotes.they expand our view of the evolutionary process and can explain the formation of mutations that confer antibiotic resistance and cancers [1]. For over 60 years, genetic experiments have shown that bacterial cells can develop mutations in the absence of growth; this is known as stationary-phase mutagenesis or stress-induced mutagenesis [1,2,3]. This type of mutagenic processes is independent of growth, and is observed in bacteria and eukaryotes. One interesting question in the stationary-phase mutagenesis field is how a bacterial population manages increases in genetic diversity without increasing the chance for genetic load. In E. coli, stressed cells have evolved mechanisms to license the increase of error-prone repair at genetic regions

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