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A component of gamma-radiation-induced cell death in E. coli is programmed and interlinked with activation of caspase-3 and SOS response

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Abstract

The current study deals with the molecular mechanism of radiation-induced cell death (RICD) in Escherichia coli. Irradiated E. coli cells displayed markers similar to those found in eukaryotic programmed cell death (PCD) such as caspase-3 activation and phosphatidylserine externalization. RICD was found to be suppressed upon pretreatment with sublethal concentrations of rifampicin or chloramphenicol, indicating the requirement of de novo gene expression. RICD was also found to be inhibited by cell permeable inhibitors of caspase-3 or poly (ADP-ribose) polymerase, indicating the involvement of PCD during RICD in E. coli. Radiation-induced SOS response was alleviated as observed with decrease in LexA level and also reduced cell filamentation frequency in the presence of caspase inhibitor. Further, the inhibitor-mediated rescue was not observed in single-gene knockouts of umuC, umuD, recB and ruvA, the genes which are associated with SOS response. This implies a linkage between SOS response and PCD in radiation-exposed E. coli cells.

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Acknowledgments

Authors acknowledge Keio collection, Japan, for E. coli knockout strains provided to our institute (Bhabha Atomic Research Centre, Mumbai, India) and our institutional colleague S. H. Mangoli for sharing these strains with us. Authors also acknowledge Prof M. Z. Humayun, UMDNJ for gifting us E. coli MG1655 strain. We also thank A. P. Janardhan for his help in performing flow cytometry as well as Dr. S. N. Jamdar and S. Hajare for their help in caspase protein characterization.

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Correspondence to Arun Sharma.

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Communicated by Jorge Membrillo-Hernandez.

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Wadhawan, S., Gautam, S. & Sharma, A. A component of gamma-radiation-induced cell death in E. coli is programmed and interlinked with activation of caspase-3 and SOS response. Arch Microbiol 195, 545–557 (2013). https://doi.org/10.1007/s00203-013-0906-6

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  • DOI: https://doi.org/10.1007/s00203-013-0906-6

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