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Mol Microbiol. 1991 Apr;5(4):933-9.

Insertional inactivation of the Staphylococcus aureus beta-toxin by bacteriophage phi 13 occurs by site- and orientation-specific integration of the phi 13 genome.

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1
School of Dental Science, University of Dublin, Trinity College, Ireland.

Abstract

Lysogenization of Staphylococcus aureus by the serotype F converting bacteriophage phi 13 results in loss of beta-toxin expression. Sequence analysis of the S. aureus beta-toxin gene (hlb), the attachment site (attP)-containing region of phi 13 DNA and the chromosome/bacteriophage DNA junctions of a phi 13 lysogen, revealed that the molecular mechanism of loss of beta-toxin expression was due to insertion of the phi 13 genome into the 5' end of hlb. The insertion site (attB) within hlb contained a 14 base pair core sequence in common with attP and both ends of the integrated linear prophage genome of a phi 13 lysogen. These findings indicate that integration of the phi 13 genome into hlb is site- and orientation-specific.

[Indexed for MEDLINE]

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