Transcription of the phage-encoded Panton-Valentine leukocidin of Staphylococcus aureus is dependent on the phage life-cycle and on the host background

• Published in: Microbiology (Society for General Microbiology) 2009-11, Vol.155 (11), p.3491-3499
• Main Authors: Wirtz, Christiane, Witte, Wolfgang, Wolz, Christiane, Goerke, Christiane
• Format: Article
• Language: English
• Subjects: Bacterial Toxins - genetics; Bacterial Toxins - metabolism; Bacteriology; Biological and medical sciences; DNA, Viral - genetics; Exotoxins - genetics; Exotoxins - metabolism; Fundamental and applied biological sciences. Psychology; Leukocidins - genetics; Leukocidins - metabolism; Methicillin-Resistant Staphylococcus aureus - genetics; Methicillin-Resistant Staphylococcus aureus - metabolism; Methicillin-Resistant Staphylococcus aureus - pathogenicity; Methicillin-Resistant Staphylococcus aureus - virology; Microbiology; Miscellaneous; Mitomycin - pharmacology; Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains; Rec A Recombinases - metabolism; Staphylococcal Infections - microbiology; Staphylococcus aureus; Staphylococcus Phages - physiology; Transcription, Genetic; Virology; Virulence; Virus Activation
• ISSN: 1350-0872; 1465-2080
• DOI: 10.1099/mic.0.032466-0

1 Institut für Medizinische Mikrobiologie und Hygiene, Universitätsklinikum Tübingen, Elfriede-Aulhorn-Str. 6, 72076 Tübingen, Germany 2 Robert-Koch-Institut Wernigerode, Burgstr. 37, 38855 Wernigerode, Germany Panton-Valentine leukocidin (PVL) is a pore-forming, bi-component toxin secreted by Staphylococcus aureus strains epidemiologically associated with diseases such as necrotizing pneumonia and skin and soft-tissue infections. Here we demonstrate that transcription of the phage-encoded PVL (encoded in the luk -PV operon) is dependent on two major determinants: the phage life-cycle and the host chromosomal background. Mitomycin C induction of PVL-encoding prophages from different community-acquired MRSA strains led to an increase in the amount of luk -PV mRNA as a result of read-through transcription from latent phage promoters and an increase in phage copy numbers. Failing prophage excision was reflected in a constant expression of luk -PV as in the case of strain USA300, suggesting that Sa2USA300 is a replication-defective prophage. Additionally, we could show that luk -PV transcription is influenced by the S. aureus global virulence regulators agr and sae . We found a strong impact of the host background on prophage induction and replication when analysing PVL phages in different S. aureus strains. For example phage Sa2mw was greatly induced by mitomycin C in its native host MW2 and in strain Newman but to a considerably lesser extent in strains 8325-4, RN6390 and ISP479c. This discrepancy was not linked to the SOS response of the bacteria since recA transcription did not vary between the strains. These results suggest a fine tuning between certain phages and their host, with major impact on the expression of phage-encoded virulence genes. Correspondence Christiane Goerke christiane.goerke{at}med.uni-tuebingen.de Abbreviations: ca, community-acquired; MRSA, meticillin-resistant Staphylococcus aureus ; MSSA, meticillin-sensitive Staphylococcus aureus ; PVL, Panton–Valentine leukocidin Related Article For CA-MRSA, how much PVL is too much? Jodi A. Lindsay Microbiology 2009 155: 3473-3474. [Full Text] [PDF]