†Present address: Wyeth–Ayerst Research, Pearl River, NY 10965, USA.
Molecular genetics of SaPI1 – a mobile pathogenicity island in Staphylococcus aureus
Article first published online: 21 DEC 2001
Volume 41, Issue 2, pages 365–377, July 2001
How to Cite
Ruzin, A., Lindsay, J. and Novick, R. P. (2001), Molecular genetics of SaPI1 – a mobile pathogenicity island in Staphylococcus aureus. Molecular Microbiology, 41: 365–377. doi: 10.1046/j.1365-2958.2001.02488.x
- Issue published online: 21 DEC 2001
- Article first published online: 21 DEC 2001
- Accepted 13 April, 2001.
The Staphylococcus aureus gene for toxic shock toxin (tst) is carried by a 15 kb mobile pathogenicity island, SaPI1, that has an intimate relationship with temperate staphylococcal phage 80α. During phage growth, SaPI1 is excised from its unique chromosomal site, attC, replicates autonomously, interferes with phage growth, and is efficiently encapsidated into special small phage heads commensurate with its size. Upon transfer to a recipient organism, SaPI1 integrates at attC by means of a self-coded integrase. One or more phage functions are required for excision, autonomous replication and encapsidation of the element and, thus, the overall relationship between SaPI1 and 80α is similar to that between coliphages P4 and P2. Among other staphylococcal phages tested, only φ13 interacts with SaPI1, inducing excision but not replication or transfer of the element.