Regulatory cascade in SaPI activation

Abstract

Staphylococcal pathogenicity islands (SaPIs) are mobile genetic elements encoding superantigens and other toxinsand are induced for excision, replication, packaging and intercell transfer by phage-encoded anti-repressors that counter the SaPI master repressor. Though SaPI induction has heretofore been assumed to be the exclusive province of helper phages, we report here the remarkable discovery that one of the SaPIs, SaPI3, can instead be induced only by a second, co-resident SaPI, which must first be induced by a phage. This induction cascade thus represents intricate regulatory triad; SaPI3, the beneficiary of this intracellular largess, is the prototype of a hitherto uniquely immobile SaPI lineage. We report that members of this lineage are controlled by a novel regulatory module and are induced by a highly conserved but previously uncharacterised SaPI protein. SaPI3 and its cousins are thus SaPI satellites, just as most other SaPIs are phage satellites.