Pfs promotes autolysis-dependent release of eDNA and biofilm formation in Staphylococcus aureus

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• 作者：Yan Bao (1)
  Xu Zhang (1)
  Qiu Jiang (1)
  Ting Xue (2)
  Baolin Sun (1)
  
  1. Department of Microbiology and Immunology ; School of Life Sciences ; University of Science and Technology of China ; Hefei ; 230027 ; Anhui ; China
  2. School of Life Science ; Anhui Agricultural University ; Hefei ; 230036 ; Anhui ; China
  
• 关键词：Staphylococcus aureus ; pfs ; Biofilm ; Autolysis ; eDNA
• 刊名：Medical Microbiology and Immunology
• 出版年：2015
• 出版时间：April 2015
• 年：2015
• 卷：204
• 期：2
• 页码：215-226
• 全文大小：1,811 KB
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• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Medical Microbiology
  Immunology
  
• 出版者：Springer Berlin / Heidelberg
• ISSN：1432-1831

文摘

Staphylococcus aureus is a major biofilm-forming pathogen, and biofilm formation remains an obstacle in the treatment of clinical S. aureus infection. Methylthioadenosine/S-adenosylhomocysteine nucleosidase (Pfs) has been implicated in methylation reactions, polyamine synthesis, vitamin synthesis, and quorum-sensing pathways. In this study, we observed that the deletion of pfs gene in S. aureus NCTC8325 reduced bacterial clumping ability and resulted in the decreased biofilm formation under both static and dynamic flow conditions in an autoinducer-2-independent manner. While the PIA amount was not affected, the pfs mutation significantly decreased the amount of eDNA present in the biofilm and the cell autolysis. Consistent with reduced autolysis, the transcription levels of the autolysin genes, lytM and atlE, were reduced in the absence of Pfs. These data suggest that Pfs promotes autolysis-dependent release of eDNA and biofilm formation in S. aureus, and our findings indicate that Pfs is a potential novel target for anti-biofilm therapy.