Abstract
Staphylococcus aureus uses two-component systems (TCSs) to adapt to stressful environmental conditions. To colonize a host, S. aureus must resist bacteriocins produced by commensal bacteria. In a comprehensive analysis using individual TCS inactivation mutants, the inactivation of two TCSs, graRS and braRS, significantly increased the susceptibility to the class I bacteriocins, nukacin ISK-1 and nisin A, and inactivation of vraSR slightly increased the susceptibility to nukacin ISK-1. In addition, two ABC transporters (BraAB and VraDE) regulated by BraRS and one transporter (VraFG) regulated by GraRS were associated with resistance to nukacin ISK-1 and nisin A. We investigated the role of these three TCSs of S. aureus in co-culture with S. warneri, which produces nukacin ISK-1, and Lactococcus lactis, which produces nisin A. When co-cultured with S. warneri or L. lactis, the braRS mutant showed a significant decrease in its population compared with the wild-type, whereas the graRS and vraSR mutants showed slight decreases. Expression of vraDE was elevated significantly in S. aureus co-cultured with nisin A/nukacin ISK-1-producing strains. These results suggest that three distinct TCSs are involved in the resistance to nisin A and nukacin ISK-1. Additionally, braRS and its related transporters played a central role in S. aureus survival in co-culture with the strains producing nisin A and nukacin ISK-1.
Highlights
Many bacteria produce antibacterial agents, called bacteriocins, which interfere with other bacteria in the bacterial community [1]
ISK-1 and Nisin A To investigate whether the VraDE expression level affects susceptibility to nisin A and nukacin ISK-1, we evaluated the susceptibility of bacitracin-pretreated S. aureus to nisin A and nukacin ISK-1 using the MIC method, as described above, and the spot-on-lawn method described elsewhere [11]
We investigated the susceptibility of two-component systems (TCSs) mutants against nisin A, and found similar results to nukacin ISK1 except that the susceptibility of the vraRS mutant to nisin A did not increase (Table 3, Figure S2)
Summary
Many bacteria produce antibacterial agents, called bacteriocins, which interfere with other bacteria in the bacterial community [1]. Bacteriocins are peptides or proteins that are ribosomally synthesized and show antimicrobial activity, mostly against bacterial species that are closely related to the producers [2]. Type A lantibiotics include two subtypes, type A(I) such as nisin A and type A(II) such as nukacin ISK-1. The mode of action of lantibiotics, especially nisin A, has been well characterized [7,8]. Nisin A exhibits pore-forming activity and the inhibition of cell wall biosynthesis. The mode of action of nukacin ISK-1 is not poreforming, but the inhibition of cell wall synthesis causes a bacteriostatic effect [10,11]. These bacteriocins are considered to affect other bacterial populations. Some bacteriocins, such as nisin A, are used as preservatives for foods and other surfaces [1]
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