Abstract
The GIL01 bacteriophage is a temperate phage that infects the insect pathogen Bacillus thuringiensis. During the lytic cycle, phage gene transcription is initiated from three promoters: P1 and P2, which control the expression of the early phage genes involved in genome replication and P3, which controls the expression of the late genes responsible for virion maturation and host lysis. Unlike most temperate phages, GIL01 lysogeny is not maintained by a dedicated phage repressor but rather by the host’s regulator of the SOS response, LexA. Previously we showed that the lytic cycle was induced by DNA damage and that LexA, in conjunction with phage-encoded protein gp7, repressed P1. Here we examine the lytic/lysogenic switch in more detail and show that P3 is also repressed by a LexA–gp7 complex, binding to tandem LexA boxes within the promoter. We also demonstrate that expression from P3 is considerably delayed after DNA damage, requiring the phage-encoded DNA binding protein, gp6. Surprisingly, gp6 is homologous to LexA itself and, thus, is a rare example of a LexA homologue directly activating transcription. We propose that the interplay between these two LexA family members, with opposing functions, ensures the timely expression of GIL01 phage late genes.
Highlights
Bacteriophages fall into two major types, depending on their developmental programmes on infecting a bacterial host cell
We investigated the regulation of the GIL01 P1 promoter and demonstrated that expression from this promoter was induced by DNA damage and that P1 was coordinately regulated by LexA and the small GIL01 phageencoded protein, gp7 (Figure 1A) [11]
When P3 expression was examined in the B. thuringiensis strain GBJ002, which has been cured of GIL01, mitomycin C-induced DNA damage failed to stimulate expression from P3, suggesting that phage-specific factors might control the P3 promoter (Figure 1C)
Summary
Bacteriophages fall into two major types, depending on their developmental programmes on infecting a bacterial host cell. Lytic phages initiate the lytic cycle immediately after infecting a cell, leading to host cell lysis and death, whereas temperate phages ( referred to as lysogenic phages) can immediately engage in the lytic cycle or lie dormant inside the host for many generations. The majority of known temperate phages insert their genomes into the host chromosome during lysogeny, where they are replicated at each cell division and are faithfully transmitted to progeny cells, whilst other lysogenic phage exist as an autonomously replicating entity. To date lysogeny has only been thoroughly studied in detail for a handful of phages, and yet it is clear that temperate bacteriophages have a great impact on bacterial evolution, leading to the rearrangement of bacterial genomes and acquisition of potent virulence determinants [1].
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