Lytic gene expression in the temperate bacteriophage GIL01 is activated by a phage-encoded LexA homologue

Research output: Contribution to journalArticlepeer-review

Authors

  • Nadine Fornelos
  • Anja Pavlin
  • Zdravko Podlesek
  • Vesna Hodnik
  • Margarita Salas
  • Matej Butala

Colleges, School and Institutes

External organisations

  • Universidad Autónoma de Madrid
  • University of Birmingham
  • University of Ljubljana

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.

Details

Original languageEnglish
Pages (from-to)9432–9443
JournalNucleic Acids Research
Volume46
Issue number18
Early online date24 Jul 2018
Publication statusPublished - 12 Oct 2018