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Changes in the transcriptome of S. aureus SH1000 containing a nisin resistance mutation in nsaS

ABSTRACT: We have demonstrated previously that high-level resistance to nisin can occur in Staphylococcus aureus as a consequence of a single non-synonymous mutation in nsaS, which encodes a putative sensor kinase. To explore the mechanism by which this mutation confers high-level resistance we compared global transcriptomes of SH1000 and SH1000 (NsaS A208E) using RNAseq. This process identified several genes to be upregulated in SH1000 (NsaS A208E), including members of the NsaRS regulon which encode VraDE and BraDE, two putative ABC-transporters and are known to provide intrinsic nisin resistance. Gene deletion and complementation experiments revealed that both BraDE and VraDE are essential to high-level nisin resistance, with BraDE required for signal transduction through NsaRS, and VraDE directly responsible for nisin detoxification.

ORGANISM(S): Staphylococcus aureus

PROVIDER: GSE114706 | GEO | 2018/11/19

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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Changes in the transcriptome of S. aureus SH1000 containing a nisin resistance mutation in nsaS

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