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.
Bibliographical note© The Author(s) 2018. Published by Oxford University Press on behalf of Nucleic Acids Research.
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Funding: Slovenian Research Agency [J1-8150 to M.B., A.P.; P1-0207 to M.B., V.H.]; Spanish Ministry of Economy and Competitiveness Grant [BFU2014-52656-P to M.S.]; Fundación Ramón Areces; Banco Santander; Industrial Biotechnology Catalyst (Innovate UK, BBSRC, EPSRC) [BB/M018261/1 to D.F.B.]; National Research Fund in Luxembourg (co-funded under the Marie Curie Actions of the European Commission) [FP7-COFUND grant PDR-09-051 to N.F.]; FEBS Short-term Fellowship (to N.F.).
- Bacillus subtilis/genetics
- Bacillus thuringiensis/genetics
- Bacterial Proteins/genetics
- Base Sequence
- Gene Expression Regulation, Viral
- Promoter Regions, Genetic
- Sequence Homology
- Serine Endopeptidases/genetics
- Transcription, Genetic/genetics
- Viral Proteins/genetics