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Insertional inactivation of the <i>Staphylococcus aureus</i>β‐toxin by bacteriophage φ13 occurs by site‐and orientation‐specific integration of the φ 13 genome
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Citations
21
References
1991
Year
Microbial PathogensBacteriologyStaphylococcus AureusMolecular BiologyBacteriophageMolecular GeneticsAnalytical UltracentrifugationBacterial PathogensSerotype Fφ 13Phage BiologyHost-pathogen InteractionsVirulence FactorPhi 13Insertional InactivationClinical MicrobiologyStructural BiologyNatural SciencesPathogenesisBacteriophage φ13MicrobiologyMedicine
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.
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