OBJECTIVES: ASABF (Ascaris suum antibacterial factor) is a CSalphabeta-type antimicrobial peptide isolated from nematodes. ASABF-alpha, a member of ASABF, is particularly effective against the gram-positive pathogen Staphylococcus aureus. In this study, we investigated the role of sigB expression on ASABF-resistance in S. aureus. METHODS: Based on preliminary characterization of the ASABF-resistant strain, Mu50, we speculated that the alternative sigma factor sigB may regulate resistance against antimicrobial peptides. To test this hypothesis, the ASABF susceptibility was compared between NKSB (a sigB-knockout derivative of N315) and its sigB-overexpressing derivative. In addition, similar experiments were carried out for N315ex, a deletion mutant of N315 for SCCmec (Staphylococcus cassette chromosome mec) which contains essential genes for beta-lactam resistance. RESULTS: The sigB-overexpressing NKSB acquired an increased resistance to ASABF-alpha compared with the parent strain. The sigB-induced ASABF-alpha resistance was also observed in N315ex. CONCLUSIONS: The overexpression of sigB confers resistance to the antimicrobial peptide, ASABF-alpha. SCCmec is not essential for this resistance.
OBJECTIVES: ASABF (Ascaris suum antibacterial factor) is a CSalphabeta-type antimicrobial peptide isolated from nematodes. ASABF-alpha, a member of ASABF, is particularly effective against the gram-positive pathogen Staphylococcus aureus. In this study, we investigated the role of sigB expression on ASABF-resistance in S. aureus. METHODS: Based on preliminary characterization of the ASABF-resistant strain, Mu50, we speculated that the alternative sigma factor sigB may regulate resistance against antimicrobial peptides. To test this hypothesis, the ASABF susceptibility was compared between NKSB (a sigB-knockout derivative of N315) and its sigB-overexpressing derivative. In addition, similar experiments were carried out for N315ex, a deletion mutant of N315 for SCCmec (Staphylococcus cassette chromosome mec) which contains essential genes for beta-lactam resistance. RESULTS: The sigB-overexpressing NKSB acquired an increased resistance to ASABF-alpha compared with the parent strain. The sigB-induced ASABF-alpha resistance was also observed in N315ex. CONCLUSIONS: The overexpression of sigB confers resistance to the antimicrobial peptide, ASABF-alpha. SCCmec is not essential for this resistance.