Ruzin A, Lindsay J, Novick R P
Skirball Institute, New York University Medical Center, 540 First Avenue, New York, NY 10016, USA.
Mol Microbiol. 2001 Jul;41(2):365-77. doi: 10.1046/j.1365-2958.2001.02488.x.
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 80alpha. 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 80alpha is similar to that between coliphages P4 and P2. Among other staphylococcal phages tested, only phi13 interacts with SaPI1, inducing excision but not replication or transfer of the element.
金黄色葡萄球菌中毒性休克毒素(tst)的基因由一个15 kb的移动致病岛SaPI1携带,该致病岛与温和型葡萄球菌噬菌体80α有着密切关系。在噬菌体生长过程中,SaPI1从其独特的染色体位点attC上切除,自主复制,干扰噬菌体生长,并被有效地包装到与其大小相称的特殊小噬菌体头部。转移到受体生物体后,SaPI1通过自身编码的整合酶整合到attC处。该元件的切除、自主复制和包装需要一种或多种噬菌体功能,因此,SaPI1与80α之间的整体关系类似于大肠杆菌噬菌体P4和P2之间的关系。在测试的其他葡萄球菌噬菌体中,只有phi13与SaPI1相互作用,诱导该元件切除,但不诱导其复制或转移。