Precisely modulated pathogenicity island interference with late phage gene transcription

Highly mobile staphylococcal pathogenicity islands (SaPIs) are the only source of toxic shock toxin and certain other superantigens, especially enterotoxin B. To promote their survival and spread, the SaPIs parasitize and interfere with certain bacteriophages. Unlike the interference of the clustered regularly interspaced short palindromic repeats (CRISPRs), the interference of SaPIs is never complete, allowing horizontal gene transfer and adaptation. We report a novel SaPI-determined interference mechanism that targets a phage gene essential for both phage and SaPI. Because SaPI is not self-destructive, it must modulate this inhibition to ensure production of its own infectious particles, as well as those of the phage, and it does so by means of a novel SaPI protein that binds to the inhibitor.