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Contribution of SOS genes to H2O2-induced apoptosis-like death in Escherichia coli

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Abstract

Hydrogen peroxide (H2O2) is a debriding agent that damages the microbial structure and function by generating various reactive oxygen species (ROS). H2O2-produced hydroxyl radical (OH∙) also exerts oxidative stress on microorganisms. The spread of antibiotic-resistance in bacteria is a serious issue worldwide, and greater efforts are needed to identify and characterize novel antibacterial mechanisms to develop new treatment strategies. Therefore, this study aimed to clarify the relationship between H2O2 and Escherichia coli and to elucidate a novel antibacterial mechanism(s) of H2O2. Following H2O2 exposure, increased levels of 8-hydroxydeoxyguanosine and malondialdehyde indicated that H2O2 accelerates oxidation of bacterial DNA and lipids in E. coli. As oxidative damage worsened, the SOS response was triggered. Cell division arrest and resulting filamentous cells were identified in cells, indicating that LexA was involved in DNA replication. It was also verified that RecA, a representative SOS gene, helps self-cleavage of LexA and acts as a bacterial caspase-like protein. Our findings also showed that dinF is essential to preserve E. coli from H2O2-induced ROS, and furthermore, demonstrated that H2O2-induced SOS response and SOS genes participate differently in guarding E. coli from oxidative stress. As an extreme SOS response is considered apoptosis-like death (ALD) in bacteria, additional experiments were performed to examine the characteristics of ALD. DNA fragmentation and membrane depolarization appeared in H2O2-treated cells, suggesting that H2O2 causes ALD in E. coli. In conclusion, our investigations revealed that ALD is a novel antibacterial mode of action(s) of H2O2 with important contributions from SOS genes.

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Abbreviations

ALD:

Apoptosis-like death

H2O2 :

Hydrogen peroxide

OH:

Hydroxyl radical

8-OHdG:

8-Hydroxydeoxyguanosine

MDA:

Malondialdehyde

MIC:

Minimum inhibitory concentrations

PBS:

Phosphate-buffered saline

PCD:

Programmed cell death

PS:

Phosphatidylserine

ROS:

Reactive oxygen species

TUNEL:

Transferase dUTP nick end labeling

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Acknowledgements

This research was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT & Future Planning (2020R1A2B5B01001905).

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HK and DGL conceived the study and designed the experiment. HK performed the experiments and collected the data. HK and DGL analyzed the data. HK wrote the manuscript.

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Correspondence to Dong Gun Lee.

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Communicated by Michael Polymenis.

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Kim, H., Lee, D.G. Contribution of SOS genes to H2O2-induced apoptosis-like death in Escherichia coli. Curr Genet 67, 969–980 (2021). https://doi.org/10.1007/s00294-021-01204-0

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