ABSTRACTInfections caused by the nosocomial pathogenStaphylococcus epidermidisfrequently develop on implanted medical devices and involve biofilm formation. Biofilms are surface-attached microbial communities that show increased resistance to drug treatment and mechanisms of innate host defense. In this study, a mutant library of the clinical isolateS. epidermidis1457 was constructed using mariner-based transposon mutagenesis. About a thousand mutants were screened, and 12 mutants were identified as significantly defective in biofilm formation. We focused on a mutant in which the transposon had inserted in a gene with unknown function,SERP0541, which is annotated as a gene encoding a GSP13-like general stress response protein. The gene was namedygs(encoding an unknowngeneralstress protein). Various stresses, including heat, pH, high osmolarity, and ethanol affected the survival of theygsmutant to a significantly higher degree than the wild-type strain and led to increased expression ofygs. Furthermore, synthesis of polysaccharide intercellular adhesin (PIA) and transcription of the PIA biosynthetic operon were significantly decreased in theygsmutant. These results are in accordance with the putative involvement ofygsin stress-response gene regulation and indicate thatygsinfluences biofilm development by controlling PIA-dependent biofilm accumulation. Moreover,ygshad a significant impact on the formation of biofilms and metastatic disease in two catheter-related rat infection models. Our study shows that theygsgene controlsS. epidermidisbiofilm accumulation and stress resistance, representing a key regulator of both structural and physiological biofilm characteristics with a significant impact on biofilm-associated infection.
THE ROLE OF GENERAL STRESS RESPONSE REGULATOR RpoS IN BIOFILM FORMATION BY ESCHERICHIA COLI IN THE PRESENCE OF PLANT POLYPHENOLS
