SRA

Bacillus thuringiensis serovar israelensis is the most widely used biopesticide for the control of insects that are vectors of animal and human diseases. Among several extrachromosomal elements, this endospore-forming entomopathogen harbours two bacteriophages, a linear DNA replicon GIL01 and a jumbo prophage on a plasmid pBtic235. Here we show that the 6-kDa protein gp7, encoded by GIL01, is a global transcription regulator of the host and delays induction of the pBtic235 prophage after DNA damage, which allows GIL01 to preferentially produce its own progeny. To coordinate the induction of the two phages, gp7 downregulates the expression of genes carried on pBtic235 and the data imply that gp7 submerges host LexA repressor for this purpose. We found that gp7 homologs of tectiviral prophages infecting human and animal pathogens also enhance LexA DNA-binding activity. Therefore we anticipate that the GIL01 take-over strategy will also be discovered for these phages. Our results provide evidence that the GIL01 prophage is an important factor in the biology of B. thuringiensis.