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Gene expression profile analysis of Staphylococcus aureus treated with nisin

ABSTRACT: Staphylococcus aureus (S. aureus) has already to be one of the most commonly identified bacteria that cause food poisoning. S. aureus colonization in humans can cause serious infections, toxinoses and life threatening diseases. The bacteriocin nisin has been extensively used as potential natural preservative in the food industry, but the overall transcriptional response mechanisms of S. aureus to nisin are still poorly understood. To detect the possible molecular mechanism of nisin against S. aureus, Affymetrix GeneChips were used to determine the global comparative transcription of S. aureus cells triggered by treatment with sub-inhibitory concentrations of nisin.

ORGANISM(S): Staphylococcus aureus

PROVIDER: GSE65750 | GEO | 2015/02/10

SECONDARY ACCESSION(S): PRJNA274941

REPOSITORIES: GEO

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Project description:The two-component system (TCS) is a specific regulatory system in bacteria and plays an important role in sensing and adapting to the environment. In this study, we evaluated the roles of TCSs in the major cariogenic pathogen Streptococcus mutans in resistance to several types of bacteriocin. In a comprehensive analysis using individual TCS mutants, we found that two novel TCSs were associated with resistance against distinct lantibiotics nisin A (class I type A[I]) and nukacin ISK-1(class I type A[II]). One TCS, SMU.659-660 (designated as NsrRS), was related to resistance against nisin A produced by Lactococcus lactis ATCC 11454. The other TCS, SMU.1146-1145 (designated as LcrRS), was related to resistance against nukacin ISK-1 produced by Staphylococcus warneri ISK-1. NsrRS induced the expression of SMU.658 (designated as NsrX), which constitutes an operon with nsrRS, in response to nisin A. Inactivation of nsrX increased susceptibility to nisin A. Additionally, NsrX expression in S. mutans increased the binding affinity to nisin A compared to a no-expression strain. LcrRS induced the expression of SMU.1148-50 (lctFEG), which encodes an ABC transporter and is located upstream of lcrRS, in response to nukacin ISK-1. Inactivation of lctFEG significantly increased susceptibility to nukacin ISK-1. Electrophoretic mobility shift assay analysis revealed that NsrR and LcrR bound directly to regions upstream of nsrX and lctFEG, respectively. This is the first report that two distinct TCSs, NsrRS and LcrRS, are independently involved in resistance to nisin A and nukacin ISK-1 in S. mutans. Total of 14 samples were analyzed. Total RNA from each test strain and control described below were labeled with Alexa FluorÂ® 555 and Alexa FluorÂ® 647, respectively, and were cohybridized on a single array. Labeling and hybridization were performed once or twice independently. UA159 wild type as control vs. UA159 with nisinA or nukacin ISK-1, UA159 wild type with nisinA or nukacin ISK-1 vs. nsrRS or lcrRS deletion mutant in UA159 with nisinA or nukacin ISK-1.

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Gene expression profile analysis of Staphylococcus aureus treated with nisin

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