The phage-related chromosomal islands of Gram-positive bacteria

Key Points Staphylococcus aureus pathogenicity islands (SaPIs) are highly mobile phage-related mobile genetic elements in staphylococci. Elements similar to SaPIs have been detected in related Gram-positive bacteria, prompting a name change to phage-related chromosomal islands (PRCIs). PRCIs are normally quiescent until they are induced by a helper phage that inactivates the repressor Stl. The mechanism of induction seems to vary between Stl molecules and requires helper phages specific for the SaPI. SaPIs are packaged by capsid proteins encoded by the helper phage, but helper phage DNA is excluded. Therefore, SaPIs can hijack the helper phage to mediate their own spread. In some cases autonomous replication of the SaPIs takes place. There are several proposed models for replication mechanisms in these SaPIs. Recently, high-frequency transfer of SaPIs to Listeria monocytogenes was demonstrated, suggesting that silent phage-mediated intergeneric transfer may be an important but, to date, unrecognized mode of horizontal gene transfer among bacteria. Phage-related chromosomal islands, which include the Staphylococcus aureus pathogenicity islands, often encode virulence factors and co-opt a helper phage to spread to other cells. Richard Novick and colleagues describe the life cycle of these genetic elements, the regulation of their mobility and their effects on helper phages. The phage-related chromosomal islands (PRCIs) were first identified in Staphylococcus aureus as highly mobile, superantigen-encoding genetic elements known as the S. aureus pathogenicity islands (SaPIs). These elements are characterized by a specific set of phage-related functions that enable them to use the phage reproduction cycle for their own transduction and inhibit phage reproduction in the process. SaPIs produce many phage-like infectious particles; their streptococcal counterparts have a role in gene regulation but may not be infectious. These elements therefore represent phage satellites or parasites, not defective phages. In this Review, we discuss the shared genetic content of PRCIs, their life cycle and their ability to be transferred across large phylogenetic distances.