Dataset Information

Extreme amyloid polymorphism in Staphylococcus aureus virulent PSM? peptides.

ABSTRACT: Members of the Staphylococcus aureus phenol-soluble modulin (PSM) peptide family are secreted as functional amyloids that serve diverse roles in pathogenicity and may be present as full-length peptides or as naturally occurring truncations. We recently showed that the activity of PSM?3, the most toxic member, stems from the formation of cross-? fibrils, which are at variance with the cross-? fibrils linked with eukaryotic amyloid pathologies. Here, we show that PSM?1 and PSM?4, involved in biofilm structuring, form canonical cross-? amyloid fibrils wherein ?-sheets tightly mate through steric zipper interfaces, conferring high stability. Contrastingly, a truncated PSM?3 has antibacterial activity, forms reversible fibrils, and reveals two polymorphic and atypical ?-rich fibril architectures. These architectures are radically different from both the cross-? fibrils formed by full-length PSM?3, and from the canonical cross-? fibrils. Our results point to structural plasticity being at the basis of the functional diversity exhibited by S. aureus PSM?s.

SUBMITTER: Salinas N

PROVIDER: S-EPMC6115460 | biostudies-literature | 2018 Aug

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Extreme amyloid polymorphism in Staphylococcus aureus virulent PSMα peptides.

Salinas Nir N Colletier Jacques-Philippe JP Moshe Asher A Landau Meytal M

Nature communications 20180829 1

Members of the Staphylococcus aureus phenol-soluble modulin (PSM) peptide family are secreted as functional amyloids that serve diverse roles in pathogenicity and may be present as full-length peptides or as naturally occurring truncations. We recently showed that the activity of PSMα3, the most toxic member, stems from the formation of cross-α fibrils, which are at variance with the cross-β fibrils linked with eukaryotic amyloid pathologies. Here, we show that PSMα1 and PSMα4, involved in biofi ...[more]

PMID: 30158633

Similar Datasets

Project description:In Australia the PVL-positive ST93-IV [2B], colloquially known as "Queensland CA-MRSA" has become the dominant CA-MRSA clone. First described in the early 2000s, ST93-IV [2B] is associated with skin and severe invasive infections including necrotizing pneumonia. A singleton by multilocus sequence typing (MLST) eBURST analysis ST93 is distinct from other S. aureus clones. To determine if the increased prevalence of ST93-IV [2B] is due to the widespread transmission of a single strain of ST93-IV [2B] the genetic relatedness of 58 S. aureus ST93 isolated throughout Australia over an extended period were studied in detail using a variety of molecular methods including pulsed-field gel electrophoresis, spa typing, MLST, microarray DNA, SCCmec typing and dru typing. Identification of the phage harbouring the lukS-PV/lukF-PV Panton Valentine leucocidin genes, detection of allelic variations in lukS-PV/lukF-PV, and quantification of LukF-PV expression was also performed. Although ST93-IV [2B] is known to have an apparent enhanced clinical virulence, the isolates harboured few known virulence determinants. All PVL-positive isolates carried the PVL-encoding phage ?Sa2USA and the lukS-PV/lukF-PV genes had the same R variant SNP profile. The isolates produced similar expression levels of LukF-PV. Although multiple rearrangements of the spa sequence have occurred, the core genome in ST93 is very stable. The emergence of ST93-MRSA is due to independent acquisitions of different dru-defined type IV and type V SCCmec elements in several spa-defined ST93-MSSA backgrounds. Rearrangement of the spa sequence in ST93-MRSA has subsequently occurred in some of these strains. Although multiple ST93-MRSA strains were characterised, little genetic diversity was identified for most isolates, with PVL-positive ST93-IVa [2B]-t202-dt10 predominant across Australia. Whether ST93-IVa [2B] t202-dt10 arose from one PVL-positive ST93-MSSA-t202, or by independent acquisitions of SCCmec-IVa [2B]-dt10 into multiple PVL-positive ST93-MSSA-t202 strains is not known.

Dataset Information

Extreme amyloid polymorphism in Staphylococcus aureus virulent PSM? peptides.

Publications

Extreme amyloid polymorphism in Staphylococcus aureus virulent PSMα peptides.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets