Cell-Surface Phenol Soluble Modulins Regulate Staphylococcus aureus Colony Spreading.

Staphylococcus aureus produces phenol-soluble modulins (PSMs), which are amphipathic small peptides with lytic activity against mammalian cells. We previously reported that PSMα1-4 stimulate S. aureus colony spreading, the phenomenon of S. aureus colony expansion on the surface of soft agar plates,...

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Main Authors: Hayato Kizaki, Yosuke Omae, Fumiaki Tabuchi, Yuki Saito, Kazuhisa Sekimizu, Chikara Kaito
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2016-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC5056675?pdf=render
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author Hayato Kizaki
Yosuke Omae
Fumiaki Tabuchi
Yuki Saito
Kazuhisa Sekimizu
Chikara Kaito
author_facet Hayato Kizaki
Yosuke Omae
Fumiaki Tabuchi
Yuki Saito
Kazuhisa Sekimizu
Chikara Kaito
author_sort Hayato Kizaki
collection DOAJ
description Staphylococcus aureus produces phenol-soluble modulins (PSMs), which are amphipathic small peptides with lytic activity against mammalian cells. We previously reported that PSMα1-4 stimulate S. aureus colony spreading, the phenomenon of S. aureus colony expansion on the surface of soft agar plates, whereas δ-toxin (Hld, PSMγ) inhibits colony-spreading activity. In this study, we revealed the underlying mechanism of the opposing effects of PSMα1-4 and δ-toxin in S. aureus colony spreading. PSMα1-4 and δ-toxin are abundant on the S. aureus cell surface, and account for 18% and 8.5% of the total amount of PSMα1-4 and δ-toxin, respectively, in S. aureus overnight cultures. Knockout of PSMα1-4 did not affect the amount of cell surface δ-toxin. In contrast, knockout of δ-toxin increased the amount of cell surface PSMα1-4, and decreased the amount of culture supernatant PSMα1-4. The δ-toxin inhibited PSMα3 and PSMα2 binding to the S. aureus cell surface in vitro. A double knockout strain of PSMα1-4 and δ-toxin exhibited decreased colony spreading compared with the parent strain. Expression of cell surface PSMα1-4, but not culture supernatant PSMα1-4, restored the colony-spreading activity of the PSMα1-4/δ-toxin double knockout strain. Expression of δ-toxin on the cell surface or in the culture supernatant did not restore the colony-spreading activity of the PSMα1-4/δ-toxin double knockout strain. These findings suggest that cell surface PSMα1-4 promote S. aureus colony spreading, whereas δ-toxin suppresses colony-spreading activity by inhibiting PSMα1-4 binding to the S. aureus cell surface.
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spelling doaj.art-a3b55c9ba9f747fe8b3f57d592cb8f712022-12-21T16:54:04ZengPublic Library of Science (PLoS)PLoS ONE1932-62032016-01-011110e016452310.1371/journal.pone.0164523Cell-Surface Phenol Soluble Modulins Regulate Staphylococcus aureus Colony Spreading.Hayato KizakiYosuke OmaeFumiaki TabuchiYuki SaitoKazuhisa SekimizuChikara KaitoStaphylococcus aureus produces phenol-soluble modulins (PSMs), which are amphipathic small peptides with lytic activity against mammalian cells. We previously reported that PSMα1-4 stimulate S. aureus colony spreading, the phenomenon of S. aureus colony expansion on the surface of soft agar plates, whereas δ-toxin (Hld, PSMγ) inhibits colony-spreading activity. In this study, we revealed the underlying mechanism of the opposing effects of PSMα1-4 and δ-toxin in S. aureus colony spreading. PSMα1-4 and δ-toxin are abundant on the S. aureus cell surface, and account for 18% and 8.5% of the total amount of PSMα1-4 and δ-toxin, respectively, in S. aureus overnight cultures. Knockout of PSMα1-4 did not affect the amount of cell surface δ-toxin. In contrast, knockout of δ-toxin increased the amount of cell surface PSMα1-4, and decreased the amount of culture supernatant PSMα1-4. The δ-toxin inhibited PSMα3 and PSMα2 binding to the S. aureus cell surface in vitro. A double knockout strain of PSMα1-4 and δ-toxin exhibited decreased colony spreading compared with the parent strain. Expression of cell surface PSMα1-4, but not culture supernatant PSMα1-4, restored the colony-spreading activity of the PSMα1-4/δ-toxin double knockout strain. Expression of δ-toxin on the cell surface or in the culture supernatant did not restore the colony-spreading activity of the PSMα1-4/δ-toxin double knockout strain. These findings suggest that cell surface PSMα1-4 promote S. aureus colony spreading, whereas δ-toxin suppresses colony-spreading activity by inhibiting PSMα1-4 binding to the S. aureus cell surface.http://europepmc.org/articles/PMC5056675?pdf=render
spellingShingle Hayato Kizaki
Yosuke Omae
Fumiaki Tabuchi
Yuki Saito
Kazuhisa Sekimizu
Chikara Kaito
Cell-Surface Phenol Soluble Modulins Regulate Staphylococcus aureus Colony Spreading.
PLoS ONE
title Cell-Surface Phenol Soluble Modulins Regulate Staphylococcus aureus Colony Spreading.
title_full Cell-Surface Phenol Soluble Modulins Regulate Staphylococcus aureus Colony Spreading.
title_fullStr Cell-Surface Phenol Soluble Modulins Regulate Staphylococcus aureus Colony Spreading.
title_full_unstemmed Cell-Surface Phenol Soluble Modulins Regulate Staphylococcus aureus Colony Spreading.
title_short Cell-Surface Phenol Soluble Modulins Regulate Staphylococcus aureus Colony Spreading.
title_sort cell surface phenol soluble modulins regulate staphylococcus aureus colony spreading
url http://europepmc.org/articles/PMC5056675?pdf=render
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