Escherichia coli mazEF-mediated cell death as a defense mechanism that inhibits the spread of phage P1

R. Hazan, H. Engelberg-Kulka*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

186 Scopus citations


The Escherichia coli gene pair mazEF is a regulatable chromosomal toxin-antitoxin module: mazF encodes a stable toxin and mazE encodes for a labile antitoxin that overcomes the lethal effect of MazF. Because MazE is labile, inhibition of mazE expression results in cell death. We studied the effect of mazEF on the development of bacteriophage P1 upon thermoinduction of the prophage P1CM clts and upon infection with virulent phage particles (P1 vir). In several E. coli strains, we showed that the ΔmazEF derivative strains produced significantly more phages than did the parent strain. In addition, upon induction of K38(P1CM clts), nearly all of the ΔmazEF mutant cells lysed; in contrast, very few of the parental mazEF + K38 cells underwent lysis. However, most of these cells did not remain viable. Thus, while the AmazEF cells die as a result of the lytic action of the phage, most of the mazEF + cells are killed by a different mechanism, apparently through the action of the chromosomal mazEF system itself. Furthermore, the introduction of lysogens into a growing non-lysogenic culture is lethal to ΔmazEF but not for mazEF+ cultures. Thus, although mazEF action causes individual cells to die, upon phage growth this is generally beneficial to the bacterial culture because it causes P1 phage exclusion from the bacterial population. These results provide additional support for the view that bacterial cultures may share some of the characteristics of multicellular organisms.

Original languageAmerican English
Pages (from-to)227-234
Number of pages8
JournalMolecular Genetics and Genomics
Issue number2
StatePublished - Sep 2004

Bibliographical note

Funding Information:
Acknowledgements We thank Dr. M. Yarmolinsky for his advice and for supplying us with P1 strains, and Dr H. Lehnherr for advice. We also thank F. R. Warshaw-Dadon (Jerusalem, Israel) for her critical reading of the manuscript. The research described here was supported by Grant No. 215/99-2 from the Israel Science Foundation, administered by the Israel Academy of Science and Humanities.


  • Bacterial programmed cell death
  • Bacteriophage P1
  • Multicellular behavior of bacteria
  • Phage exclusion


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