rexB of bacteriophage λ is an anti-cell death gene

Hanna Engelberg-Kulka, Myriam Reches, Sudarsan Narasimhan, Rachel Schoulaker-Schwarz, Yoel Klemes, Einat Aizenman, Gad Glaser

Research output: Contribution to journalArticlepeer-review


In Escherichia coli, programmed cell death is mediated through 'addiction modules' consisting of two genes; the product of one gene is long- lived and toxic, whereas the product of the other is short-lived and antagonizes the toxic effect. Here we show that the product of λrexB, one of the few genes expressed in the lysogenic state of bacteriophage λ, prevents cell death directed by each of two addiction modules, phd-doc of plasmid prophage P1 and the rel mazEF of E. coli, which is induced by the signal molecule guanosine 3',5'-bispyrophosphate (ppGpp) and thus by amino acid starvation. λRexB inhibits the degradation of the antitoxic labile components Phd and Maze of these systems, which are substrates of ClpP proteases. We present a model for this anti-cell death effect of λRexB through its action on the ClpP proteolytic subunit. We also propose that the λrex operon has an additional function to the well known phenomenon of exclusion of other phages; it can prevent the death of lysogenized cells under conditions of nutrient starvation. Thus, the rex operon may be considered as the 'survival operon' of phage λ.

Original languageEnglish
Pages (from-to)15481-15486
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number26
StatePublished - 22 Dec 1998


  • Addiction modules
  • Programmed cell death
  • Protein degradation


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