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Cell-Surface Phenol Soluble Modulins Regulate Staphylococcus aureus Colony Spreading.
Hayato Kizaki1, Yosuke Omae1, Fumiaki Tabuchi1
1Laboratory of Microbiology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Plos One
|October 11, 2016
Summary
Phenol-soluble modulins (PSMs) on Staphylococcus aureus cell surfaces promote colony spreading. Delta-toxin suppresses this spreading by inhibiting PSM binding, revealing a key mechanism in bacterial expansion.
Area of Science:
- Microbiology
- Molecular Biology
- Bacterial Pathogenesis
Background:
- Staphylococcus aureus utilizes phenol-soluble modulins (PSMs) for various functions, including colony spreading.
- PSMα1-4 peptides stimulate S. aureus colony spreading, while δ-toxin (Hld, PSMγ) inhibits it.
- The precise mechanisms behind these opposing effects on colony spreading were previously unclear.
Purpose of the Study:
- To elucidate the underlying mechanisms of how PSMα1-4 and δ-toxin differentially regulate Staphylococcus aureus colony spreading.
- To investigate the roles of cell surface-associated and secreted PSMs in colony spreading.
Main Methods:
- Comparative analysis of wild-type, PSMα1-4 knockout, δ-toxin knockout, and double knockout S. aureus strains.
- Quantification of cell surface and supernatant PSM levels using various techniques.
- In vitro binding assays to assess the interaction between δ-toxin and PSMα peptides.
- Functional assays measuring S. aureus colony spreading on soft agar plates.
Main Results:
- δ-toxin knockout increased cell surface PSMα1-4 and decreased secreted PSMα1-4, indicating an interaction.
- δ-toxin inhibited the binding of PSMα2 and PSMα3 to the S. aureus cell surface in vitro.
- A double knockout strain showed reduced colony spreading, which was restored by expressing cell surface PSMα1-4 but not secreted PSMα1-4.
- Restoring δ-toxin expression did not rescue colony spreading in the double knockout strain.
Conclusions:
- Cell surface-localized PSMα1-4 are crucial for promoting Staphylococcus aureus colony spreading.
- δ-toxin suppresses colony spreading primarily by inhibiting the cell surface binding of PSMα1-4.
- This study reveals a novel regulatory mechanism controlling bacterial motility and expansion via peptide-surface interactions.
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