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Phase Variation of Poly-N-Acetylglucosamine Expression in


Staphylococcal polysaccharide intercellular adhesin (PIA), also known as β-1-6-linked N-acetylglucosamine (PNAG) plays a role in immune evasion and biofilm formation. Evidence suggests that under certain circumstances PIA/PNAG production is beneficial, whereas at times, it may be advantageous for the bacteria to turn production off. In S. epidermidis, PIA/PNAG can be switched off when an insertion sequence recombines into the intercellular adhesin locus (ica). In this study, we have found a short tandem repeat sequence in the ica locus of S. aureus that can undergo expansion and contraction. The addition or subtraction of non-multiples of three of this repeat shifts the reading frame of the icaC gene, resulting in the complete loss of PIA/PNAG production. We hypothesize that certain conditions that make the PIA/PNAG-negative phenotype advantageous during infection, such as the development of an effective immune response to PIA/PNAG on the bacterial surface, would select for repeat mutants. In support of this hypothesis, we found clinical isolates with expansion and deletion of the repeat. These findings reveal a new on-off switch for the expression of PIA/PNAG.


Vyšlo v časopise: Phase Variation of Poly-N-Acetylglucosamine Expression in. PLoS Pathog 10(7): e32767. doi:10.1371/journal.ppat.1004292
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1004292

Souhrn

Staphylococcal polysaccharide intercellular adhesin (PIA), also known as β-1-6-linked N-acetylglucosamine (PNAG) plays a role in immune evasion and biofilm formation. Evidence suggests that under certain circumstances PIA/PNAG production is beneficial, whereas at times, it may be advantageous for the bacteria to turn production off. In S. epidermidis, PIA/PNAG can be switched off when an insertion sequence recombines into the intercellular adhesin locus (ica). In this study, we have found a short tandem repeat sequence in the ica locus of S. aureus that can undergo expansion and contraction. The addition or subtraction of non-multiples of three of this repeat shifts the reading frame of the icaC gene, resulting in the complete loss of PIA/PNAG production. We hypothesize that certain conditions that make the PIA/PNAG-negative phenotype advantageous during infection, such as the development of an effective immune response to PIA/PNAG on the bacterial surface, would select for repeat mutants. In support of this hypothesis, we found clinical isolates with expansion and deletion of the repeat. These findings reveal a new on-off switch for the expression of PIA/PNAG.


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Hygiena a epidemiológia Infekčné lekárstvo Laboratórium

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