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首页> 外文期刊>The Journal of Antimicrobial Chemotherapy >SmQnrR, a DeoR-type transcriptional regulator, negatively regulates the expression of Smqnr and SmtcrA in Stenotrophomonas maltophilia.
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SmQnrR, a DeoR-type transcriptional regulator, negatively regulates the expression of Smqnr and SmtcrA in Stenotrophomonas maltophilia.

机译：SmQnrR，一种DeoR类型的转录调节因子，在嗜麦芽窄食单胞菌中负调节Smqnr和SmtcrA的表达。

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摘要

OBJECTIVES: To characterize the role of SmqnrR in the expression of Smqnr and SmtcrA, and the role of SmtcrA in drug resistance in Stenotrophomonas maltophilia. METHODS: SmqnrR, a DeoR-type regulator gene, is situated between a quinolone resistance gene (Smqnr) and a putative major facilitator superfamily transmembrane transporter gene (SmtcrA). To assess the regulatory role of SmQnrR in the expression of Smqnr and SmtcrA, the transcripts of Smqnr and SmtcrA genes were determined in the wild-type KJ and the SmqnrR isogenic mutant KJDeltaQnrR. An SmqnrR polar mutant, KJDeltaQnrROmega, was constructed to investigate the possibility that SmqnrR and SmtcrA form an operon. The contribution of Smqnr and SmtcrA genes to the intrinsic and acquired resistance of S. maltophilia was evaluated using susceptibility testing. RESULTS: SmQnrR acted as a repressor for the expression of Smqnr and SmtcrA genes. SmqnrR and SmtcrA genes formed an operon, which was negatively autoregulated by SmQnrR. Smqnr and SmtcrA contributed only slightly to intrinsic resistance in S. maltophilia. Nevertheless, overexpression of Smqnr and SmtcrA by inactivating SmqnrR conferred a slight increase in quinolone MICs and a more marked increase in tetracycline MIC. CONCLUSIONS: The SmQnrR protein is a transcriptional repressor for the contiguous Smqnr and SmtcrA genes, and SmQnrR is a negative regulator of SmqnrR-SmtcrA operon expression. Inactivation of SmqnrR contributes to an acquired increase in quinolone and tetracycline MICs for S. maltophilia.
机译：目的：表征SmqnrR在Smqnr和SmtcrA表达中的作用，以及SmtcrA在嗜麦芽窄食单胞菌的耐药性中的作用。方法：SmqnrR，一种DeoR型调节基因，位于喹诺酮抗性基因（Smqnr）和推定的主要促进者超家族跨膜转运蛋白（SmtcrA）之间。为了评估SmQnrR在Smqnr和SmtcrA表达中的调控作用，在野生型KJ和SmqnrR等基因突变体KJDeltaQnrR中确定了Smqnr和SmtcrA基因的转录本。构建了一个SmqnrR极性突变体KJDeltaQnrROmega，以研究SmqnrR和SmtcrA形成操纵子的可能性。使用药敏试验评估了Smqnr和SmtcrA基因对嗜麦芽糖杆菌的固有抗性和获得性抗性的贡献。结果：SmQnrR充当Smqnr和SmtcrA基因表达的阻遏物。 SmqnrR和SmtcrA基因形成操纵子，该操纵子被SmQnrR负自动调节。 Smqnr和SmtcrA对嗜麦芽胞杆菌的内在抗性仅贡献很小。但是，通过灭活SmqnrR来过度表达Smqnr和SmtcrA会导致喹诺酮类MIC略微增加，而四环素MIC则显着增加。结论：SmQnrR蛋白是连续Smqnr和SmtcrA基因的转录阻遏物，而SmQnrR是SmqnrR-SmtcrA操纵子表达的负调控子。 SmqnrR的失活导致喹诺酮和四环素MICs嗜麦芽胞杆菌的获得性增加。

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