Abstract

Inactivation of bacteriophage lambda CI repressor leads almost exclusively to lytic development. Prophage induction can be initiated either by DNA damage or by heat treatment of a temperature-sensitive repressor. These two treatments also cause a concurrent activation of either the host SOS or heat-shock stress responses respectively. We studied the effects of these two methods of induction on the lytic pathway by monitoring the activation of different lambda promoters, and found that the lambda genetic network co-ordinates information from the host stress response networks. Our results show that the function of the CII transcriptional activator, which facilitates the lysogenic developmental pathway, is not observed following either method of induction. Mutations in the cro gene restore the CII function irrespective of the induction method. Deletion of the heat-shock protease gene ftsH can also restore CII function following heat induction but not following SOS induction. Our findings highlight the importance of the elimination of CII function during induction as a way to ensure an efficient lytic outcome. We also show that, despite the common inhibitory effect on CII function, there are significant differences in the heat- and SOS-induced pathways leading to the lytic cascade.

Highlights

  • Temperate bacteriophage lambda exists in a symbiotic relationship with its host and can undergo either lytic or lysogenic development (Campbell, 2003; Livny and Friedman, 2004; Ptashne, 2004; Dodd et al, 2005) (Fig. 1A)

  • We studied the effects of these two methods of induction on the lytic pathway by monitoring the activation of different lambda promoters, and found that the lambda genetic network co-ordinates information from the host stress response networks

  • Our results show that the function of the CII transcriptional activator, which facilitates the lysogenic developmental pathway, is not observed following either method of induction

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Summary

Introduction

Temperate bacteriophage lambda exists in a symbiotic relationship with its host and can undergo either lytic or lysogenic development (Campbell, 2003; Livny and Friedman, 2004; Ptashne, 2004; Dodd et al, 2005) (Fig. 1A). The highly stable lysogenic state, in which the prophage replicates passively with the host genome, is maintained by the expression of the CI repressor that by binding at the oL and oR operators, blocks the cascade of phage lytic gene expression. Treatment with DNA-damaging agents can lead to activation of the host SOS response, a DNA repair system induced by DNA damage. This results in the inactivation of the CI repressor and in an irreversible switch into lytic development (Campbell, 2003; Ptashne, 2004). In both the infection and induction processes, the lCro protein partially represses the pL and pR promoters, and its activity is required for efficient lytic growth (Svenningsen et al, 2005)

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