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Journal of Bacteriology, February 2004, p. 866-869, Vol. 186, No. 3
0021-9193/04/$08.00+0     DOI: 10.1128/JB.186.3.866-869.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Transcriptional Profiling of Colicin-Induced Cell Death of Escherichia coli MG1655 Identifies Potential Mechanisms by Which Bacteriocins Promote Bacterial Diversity

Department of Biology, University of York, Heslington, York YO10 5YW,¹ Molecular Microbiology Group, Institute of Food Research, Norwich Research Park, Colney, Norwich NR4 7UA,² School of Chemical Sciences and Pharmacy, University of East Anglia, Norwich NR4 7TJ,³ Division of Microbiology & Infectious Diseases, University Hospital, Queens Medical Centre, University of Nottingham, Nottingham NG7 2UH, United Kingdom⁴

Received 28 August 2003/ Accepted 24 October 2003

We report the transcriptional response of Escherichia coli MG1655 to damage induced by colicins E3 and E9, bacteriocins that kill cells through inactivation of the ribosome and degradation of chromosomal DNA, respectively. Colicin E9 strongly induced the LexA-regulated SOS response, while colicin E3 elicited a broad response that included the induction of cold shock genes, symptomatic of translational arrest. Colicin E3 also increased the transcription of cryptic prophage genes and other laterally acquired mobile elements. The transcriptional responses to both these toxins suggest mechanisms that may promote genetic diversity in E. coli populations, pointing to a more general role for colicins in adaptive bacterial physiology than has hitherto been realized.

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