The alternative sigma factor SigH modulates biofilm formation and stress tolerance in a raw milk-derived Staphylococcus aureus.
TL;DR
Findings indicate that SigH contributes to the regulation of persistence-associated phenotypes in a raw milk-derived S. aureus strain and provide new insights into the regulatory mechanisms that may influence survival of this pathogen in dairy-related environments.
Abstract
Staphylococcus aureus is an important raw milk contaminant that can persist in dairy environments through biofilm formation and adaptation to environmental stresses. Although the alternative sigma factor SigH has been described in S. aureus, its role in raw milk-associated strains remains poorly understood. In this study, we investigated the function of SigH in the raw milk-derived S. aureus strain RMSA24 in biofilm formation, stress tolerance and antibiotic susceptibility. Deletion of sigH did not affect bacterial growth under routine culture conditions but significantly reduced biofilm formation. In contrast, the sigH mutant exhibited enhanced tolerance to osmotic, acid, and heat stresses. Loss of sigH also reduced susceptibility to the glycopeptide antibiotics vancomycin and teicoplanin and was accompanied by pronounced cell wall thickening. Transcriptomic analysis further supported these phenotypes by revealing differential expression of genes associated with biofilm formation, stress tolerance, and cell wall homeostasis. Overall, these findings indicate that SigH contributes to the regulation of persistence-associated phenotypes in a raw milk-derived S. aureus strain and provide new insights into the regulatory mechanisms that may influence survival of this pathogen in dairy-related environments.