Control of Staphylococcus aureus pathogenicity island excision.

Area of Science:

• Microbiology
• Molecular Biology
• Genetics

Background:

• Staphylococcus aureus pathogenicity islands (SaPIs) are mobile genetic elements encoding virulence factors.
• SaPIs utilize phage-induced replication and encapsidation for mobility.
• Chromosomal integration is mediated by the SaPI-encoded Int recombinase.

Purpose of the Study:

• To investigate the mechanism of SaPI excision from the host chromosome.
• To identify the role of SaPI-encoded proteins in excision and horizontal transfer.
• To elucidate the regulatory control of SaPI excision.

Main Methods:

• In vivo recombination assays using plasmids in Escherichia coli.
• Site-specific and mutational analyses of SaPI att sites and flanking sequences.
• Investigation of the Stl regulator's role in controlling int and xis gene expression.

Main Results:

• SaPI-encoded Xis protein is essential for recombination between SaPI att(L) and att(R) sites.
• Both att sites and flanking SaPI sequences are necessary for efficient SaPI excision.
• Xis is critical for the horizontal transfer of SaPIs to recipient strains.
• The Stl regulator binds to inverted repeats, inhibiting int and xis expression and controlling SaPI excision.

Conclusions:

• SaPI excision and transfer are dependent on SaPI-encoded Int and Xis proteins.
• SaPIs encode their own Xis function, crucial for their mobility.
• The Stl regulator acts as a master switch, controlling SaPI excision by regulating int and xis expression.