Staphylococcus aureus skin colonization is mediated by SasG lectin variation

Area of Science:

• Microbiology
• Molecular Biology
• Dermatology

Background:

• Staphylococcus aureus is a primary cause of skin and soft tissue infections.
• Transient skin colonization by S. aureus precedes infection.
• Surface protein G (SasG) mediates initial S. aureus adhesion to skin corneocytes.

Purpose of the Study:

• To investigate the structural and functional diversity of Staphylococcus aureus surface protein G (SasG) alleles.
• To elucidate the molecular mechanisms underlying SasG-mediated bacterial adhesion to skin cells.

Main Methods:

• Phylogenetic analysis of SasG alleles.
• Structural analysis of SasG-II.
• Atomic force microscopy and corneocyte adhesion assays.
• Glycosidase treatment and N/TERT keratinocyte binding studies.

Main Results:

• Two major divergent SasG alleles, SasG-I and SasG-II, were identified in S. aureus.
• SasG-II possesses a unique structural feature in its lectin subdomain binding pocket.
• SasG-II exhibits broader ligand-binding capabilities compared to SasG-I on skin cells.
• Differential binding profiles were observed between SasG-I and SasG-II following glycosidase treatment.

Conclusions:

• SasG-II has evolved enhanced adhesive properties for broader ligand interaction.
• This broader adhesion confers a significant advantage to S. aureus during skin colonization.
• Understanding SasG variants can inform strategies to prevent S. aureus skin infections.