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Molecular genetics of SaPI1 – a mobile pathogenicity island in Staphylococcus aureus
Alexey Ruzin Jodi Lindsay Richard P. Novick*
Skirball Institute, New York University Medical Center, 540 First Avenue, New York, NY 10016, USA
*For correspondence. E-mail novick@saturn.med.nyu.edu; Tel. (+1) 212 263 6290; Fax (+1) 212 263 5711.
 

Present address: Wyeth–Ayerst Research, Pearl River, NY 10965, USA.

 

Present address: St. George's Hospital Medical School, London, UK.

Copyright Blackwell Science Ltd

ABSTRACT

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.


Accepted 13 April, 2001.

DIGITAL OBJECT IDENTIFIER (DOI)
10.1046/j.1365-2958.2001.02488.x About DOI

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