scholarly journals Inducible Expression of a Resistance-Nodulation-Division-Type Efflux Pump in Staphylococcus aureus Provides Resistance to Linoleic and Arachidonic Acids

2015 ◽  
Vol 197 (11) ◽  
pp. 1893-1905 ◽  
Author(s):  
Heba Alnaseri ◽  
Benjamin Arsic ◽  
James E. T. Schneider ◽  
Julienne C. Kaiser ◽  
Zachariah C. Scinocca ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Staphylococcus Aureus ◽  
Linoleic Acid ◽  
Defense Mechanisms ◽  
Efflux Pump ◽  
Content Type ◽  
Inducible Resistance ◽  
Resistance Nodulation Division ◽  
Y Substitution ◽  
Arachidonic Acids

ABSTRACTAlthoughStaphylococcus aureusis exposed to antimicrobial fatty acids on the skin, in nasal secretions, and in abscesses, a specific mechanism of inducible resistance to this important facet of innate immunity has not been identified. Here, we have sequenced the genome ofS. aureusUSA300 variants selected for their ability to grow at an elevated concentration of linoleic acid. The fatty acid-resistant clone FAR7 had a single nucleotide polymorphism resulting in an H121Y substitution in an uncharacterized transcriptional regulator belonging to the AcrR family, which was divergently transcribed from a gene encoding a member of the resistance-nodulation-division superfamily of multidrug efflux pumps. We named these genesfarRandfarE, forregulator andeffector offattyacidresistance, respectively. Several lines of evidence indicated that FarE promotes efflux of antimicrobial fatty acids and is regulated by FarR. First, expression offarEwas strongly induced by arachidonic and linoleic acids in anfarR-dependent manner. Second, an H121Y substitution in FarR resulted in increased expression offarEand was alone sufficient to promote increased resistance ofS. aureusto linoleic acid. Third, inactivation offarEresulted in a significant reduction in the inducible resistance ofS. aureusto the bactericidal activity of 100 μM linoleic acid, increased accumulation of [14C]linoleic acid by growing cells, and severely impaired growth in the presence of nonbactericidal concentrations of linoleic acid. Cumulatively, these findings represent the first description of a specific mechanism of inducible resistance to antimicrobial fatty acids in a Gram-positive pathogen.IMPORTANCEStaphylococcus aureuscolonizes approximately 25% of humans and is a leading cause of human infectious morbidity and mortality. To persist on human hosts,S. aureusmust have intrinsic defense mechanisms to cope with antimicrobial fatty acids, which comprise an important component of human innate defense mechanisms. We have identified a novel pair of genes,farRandfarE, that constitute a dedicated regulator and effector ofS. aureusresistance to linoleic and arachidonic acids, which are major fatty acids in human membrane phospholipid. Expression offarE, which encodes an efflux pump, is induced in anfarR-dependent mechanism, in response to these antimicrobial fatty acids that would be encountered in a tissue abscess.

scholarly journals Novel Functions and Signaling Specificity for the GraS Sensor Kinase of Staphylococcus aureus in Response to Acidic pH

2020 ◽  
Vol 202 (22) ◽  
Author(s):  
Robert C. Kuiack ◽  
Ruud A. W. Veldhuizen ◽  
Martin J. McGavin
Keyword(s):  
Fatty Acids ◽  
Staphylococcus Aureus ◽  
Cell Surface ◽  
Antimicrobial Peptides ◽  
Sensor Kinase ◽  
Acidic Ph ◽  
Content Type ◽  
Enhanced Resistance ◽  
Secreted Proteases ◽  
Arachidonic Acids

ABSTRACT Although the GraS sensor kinase of Staphylococcus aureus is known for the sensing of and resistance to cationic antimicrobial peptides (CAMPs), we recently established that it also signals in response to acidic pH, which is encountered on human skin concurrently with CAMPs, antimicrobial unsaturated free fatty acids (uFFA), and calcium. We therefore evaluated how these environmental signals would affect GraS function and resistance to antimicrobial uFFA. Growth at pH 5.5 promoted increased resistance of S. aureus USA300 to linoleic and arachidonic acids but not palmitoleic or sapienic acid. However, enhanced resistance to these C16:1 uFFA was achieved by supplementing acidic medium with 0.5 mM calcium or subinhibitory CAMPs. Enhanced resistance to uFFA at acidic pH was dependent on GraS and GraS-dependent expression of the lysyl-phosphatidylglycerol synthase enzyme MprF, through a mechanism that did not require the lysyl-transferase function of MprF. In addition to enhanced resistance to antimicrobial uFFA, acidic pH also promoted increased production of secreted proteases in a GraS-dependent manner. During growth at pH 5.5, downstream phenotypes of signaling through GraS, including resistance to uFFA, MprF-dependent addition of positive charge to the cell surface, and increased production of secreted proteases, all occurred independently of acidic amino acids in the extracytoplasmic sensor loop of GraS that were previously found to be required for sensing of CAMPs. Cumulatively, our data indicate that signaling through GraS at acidic pH occurs through a mechanism that is distinct from that described for CAMPs, leading to increased resistance to antimicrobial uFFA and production of secreted proteases. IMPORTANCE Staphylococcus aureus asymptomatically colonizes 30% of humans but is also a leading cause of infectious morbidity and mortality. Since infections are typically initiated by the same strain associated with asymptomatic colonization of the nose or skin, it is important to understand how the microbe can endure exposure to harsh conditions that successfully restrict the growth of other bacteria, including a combination of acidic pH, antimicrobial peptides, and antimicrobial fatty acids. The significance of our research is in showing that acidic pH combined with antimicrobial peptide or environmental calcium can signal through a single membrane sensor protein to promote traits that may aid in survival, including modification of cell surface properties, increased resistance to antimicrobial fatty acids, and enhanced production of secreted proteases.

scholarly journals Role of the Tet38 Efflux Pump in Staphylococcus aureus Internalization and Survival in Epithelial Cells

2015 ◽  
Vol 83 (11) ◽  
pp. 4362-4372 ◽  
Author(s):  
Q. C. Truong-Bolduc ◽  
G. R. Bolduc ◽  
H. Medeiros ◽  
J. M. Vyas ◽  
Y. Wang ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Staphylococcus Aureus ◽  
Epithelial Cells ◽  
Unsaturated Fatty Acids ◽  
Efflux Pump ◽  
Fold Increase ◽  
Growth Patterns ◽  
Heart Cell ◽  
Content Type

ABSTRACTWe previously identified the protein Tet38 as a chromosomally encoded efflux pump ofStaphylococcus aureusthat confers resistance to tetracycline and certain unsaturated fatty acids. Tet38 also contributes to mouse skin colonization. In this study, we discovered a novel regulator oftet38, named tetracycline regulator 21 (TetR21), that bound specifically to thetet38promoter and repressed pump expression. A ΔtetR21mutant showed a 5-fold increase intet38transcripts and an 8-fold increase in resistance to tetracycline and fatty acids. The global regulator MgrA bound to thetetR21promoter and indirectly repressed the expression oftet38. To further assess the full role of Tet38 inS. aureusadaptability, we tested its effect on host cell invasion using A549 (lung) and HMEC-1 (heart) cell lines. We usedS. aureusRN6390, its Δtet38, ΔtetR21, and ΔmgrAmutants, and a Δtet38 ΔtetR21double mutant. After 2 h of contact, the Δtet38mutant was internalized in 6-fold-lower numbers than RN6390 in A549 and HMEC-1 cells, and the ΔtetR21mutant was internalized in 2-fold-higher numbers than RN6390. A slight increase of 1.5-fold in internalization was found for the ΔmgrAmutant. The growth patterns of RN6390 and the ΔmgrAand ΔtetR21mutants within A549 cells were similar, while no growth was observed for the Δtet38mutant. These data indicate that the Tet38 efflux pump is regulated by TetR21 and contributes to the ability ofS. aureusto internalize and replicate within epithelial cells.

Olive or salmon oils affect differently the storage and transport of fatty acids by VLDL in hypercholesterolemic rats fed different proteins

2016 ◽  
Vol 46 (2) ◽  
pp. 190-203 ◽  
Author(s):  
Sherazede Bouderbala ◽  
Malika Bouchenak
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Linoleic Acid ◽  
Acid Content ◽  
Phospholipid Fatty Acid ◽  
Linoleic Acid Content ◽  
Arachidonic Acid Content ◽  
Oleic Acid Content ◽  
Content Type ◽  
Arachidonic Acids

Purpose – The purpose of this study is to compare the effect of olive or salmon oil on the hepatic storage and transport of fatty acids by very-low-density lipoproteins (VLDL). Design/methodology/approach – In all, 24 male Wistar rats (80 ± 5 g) were fed a 0.5 per cent cholesterol-enriched diet with either 20 per cent casein (C) or chickpea (CP) proteins with 10 per cent olive (O) or salmon (S) oil for 28 days. Findings – In VLDL-triacyglycerols fatty acids, oleic acid content was higher in CPS as compared to that in CS or CPO and lower in CS and CPO than that in CO; linoleic acid content was higher in all groups; arachidonic acid content was higher in CS and CPO as compared to that in CO. In the liver, TG fatty acids content was lower in CPO or CPS as compared to that in CO or CS; oleic and arachidonic acid contents were lower in CPS than that in CPO; linoleic acid content was lower in CS, CPS and CPO than that in CO, CPO and CO. In liver, phospholipid fatty acid, oleic and arachidonic acid contents were lower in CPS than that in CS; oleic, linoleic and arachidonic acid contents were lower in CPO compared to that in CO. In liver, cholesteryl esters fatty acids, oleic, linoleic and arachidonic acids contents were higher in CPS as compared to that in CS; oleic, linoleic and arachidonic acid contents were lower in CS as compared to that in CO; linoleic and arachidonic acid contents were lower in CPS than that in CPO. Originality/value – A cholesterol-enriched diet containing casein or chickpea proteins combined with olive or salmon oil affects the hepatic storage and transport of polyunsaturated and monounsaturated fatty acids by VLDL.

scholarly journals DNA Binding and Sensor Specificity of FarR, a Novel TetR Family Regulator Required for Induction of the Fatty Acid Efflux Pump FarE in Staphylococcus aureus

2018 ◽  
Vol 201 (3) ◽  
Author(s):  
Heba Alnaseri ◽  
Robert C. Kuiack ◽  
Katherine A. Ferguson ◽  
James E. T. Schneider ◽  
David E. Heinrichs ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Staphylococcus Aureus ◽  
Fatty Acid ◽  
Dna Binding ◽  
Unsaturated Fatty Acids ◽  
Efflux Pump ◽  
Ectopic Expression ◽  
Exogenous Fatty Acid ◽  
Content Type ◽  
Tetr Family Regulator

ABSTRACT Divergent genes in Staphylococcus aureus USA300 encode the efflux pump FarE and TetR family regulator FarR, which confer resistance to antimicrobial unsaturated fatty acids. To study their regulation, we constructed USA300 ΔfarER, which exhibited a 2-fold reduction in MIC of linoleic acid. farE expressed from its native promoter on pLIfarE conferred increased resistance to USA300 but not USA300 ΔfarER. Complementation of USA300 ΔfarER with pLIfarR also had no effect, whereas resistance was restored with pLIfarER or through ectopic expression of farE. In electrophoretic mobility shift assays, FarR bound to three different oligonucleotide probes that each contained a TAGWTTA motif, occurring as (i) a singular motif overlapping the −10 element of the PfarR promoter, (ii) in palindrome PAL1 immediately in the 3′ direction of PfarR, or (iii) within PAL2 upstream of the predicted PfarE promoter. FarR autorepressed its expression through cooperative binding to PAL1 and the adjacent TAGWTTA motif in PfarR. Consistent with reports that S. aureus does not metabolize fatty acids through acyl coenzyme A (acyl-CoA) intermediates, DNA binding activity of FarR was not affected by linoleoyl-CoA. Conversely, induction of farE required fatty acid kinase FakA, which catalyzes the first metabolic step in the incorporation of unsaturated fatty acids into phospholipid. We conclude that FarR is needed to promote the expression of farE while strongly autorepressing its own expression, and our data are consistent with a model whereby FarR interacts with a FakA-dependent product of exogenous fatty acid metabolism to ensure that efflux only occurs when the metabolic capacity for incorporation of fatty acid into phospholipid is exceeded. IMPORTANCE Here, we describe the DNA binding and sensor specificity of FarR, a novel TetR family regulator (TFR) in Staphylococcus aureus. Unlike the majority of TFRs that have been characterized, which function to repress a divergently transcribed gene, we find that FarR is needed to promote expression of the divergently transcribed farE gene, encoding a resistance-nodulation-division (RND) family efflux pump that is induced in response to antimicrobial unsaturated fatty acids. Induction of farE was dependent on the function of the fatty acid kinase FakA, which catalyzes the first metabolic step in the incorporation of exogenous unsaturated fatty acids into phospholipid. This represents a novel example of TFR function.

scholarly journals Transcriptional Profiling Analysis of the Global Regulator NorG, a GntR-Like Protein of Staphylococcus aureus

2011 ◽  
Vol 193 (22) ◽  
pp. 6207-6214 ◽  
Author(s):  
Q. C. Truong-Bolduc ◽  
P. M. Dunman ◽  
T. Eidem ◽  
D. C. Hooper
Keyword(s):  
Staphylococcus Aureus ◽  
Target Genes ◽  
Efflux Pump ◽  
Transcriptional Profiling ◽  
Fold Increase ◽  
Regulatory Function ◽  
Drug Transporter ◽  
Content Type ◽  
Global Regulators ◽  
Inorganic Ion

The GntR-like protein NorG has been shown to affectStaphylococcus aureusgenes involved in resistance to quinolones and β-lactams, such as those encoding the NorB and AbcA transporters. To identify the target genes regulated by NorG, we carried out transcriptional-profiling assays usingS. aureusRN6390 and its isogenicnorG::catmutant. Our data showed that NorG positively affected the transcription of global regulatorsmgrA,arlS, andsarZ. The three putative drug efflux pump genes most positively affected by NorG were the NorB efflux pump (5.1-fold), the MmpL-like protein SACOL2566 (5.2-fold), and the BcrA-like drug transporter SACOL2525 (5.7-fold) genes. TheS. aureuspredicted MmpL protein showed 53% homology with the MmpL lipid transporter ofMycobacterium tuberculosis, and the putative SACOL2525 protein showed 87% homology with the bacitracin drug transporter BcrA ofStaphylococcus hominis. Two pump genes most negatively affected by NorG were the NorC (4-fold) and AbcA (6-fold) genes. Other categories of genes, such as those participating in amino acid, inorganic ion, or nucleotide transporters and metabolism, were also affected by NorG. Real-time reverse transcription (RT)-PCR assays formgrA,arlS,sarZ,norB,norC,abcA,mmpL, andbcrA-like were carried out to verify microarray data and showed the same level of up- or downregulation by NorG. ThenorGmutant showed a 2-fold increase in resistance to norfloxacin and rhodamine, both substrates of the NorC transporter, which is consistent with the resistance phenotype conferred by overexpression ofnorCon a plasmid. These data indicate that NorG has broad regulatory function inS. aureus.

scholarly journals Systematic Analysis of Efflux Pump-Mediated Antiseptic Resistance in Staphylococcus aureus Suggests a Need for Greater Antiseptic Stewardship

mSphere ◽  
2020 ◽  
Vol 5 (1) ◽  
Author(s):  
Patrick T. LaBreck ◽  
Audrey C. Bochi-Layec ◽  
Joshua Stanbro ◽  
Gina Dabbah-Krancher ◽  
Mark P. Simons ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Efflux Pump ◽  
Efflux Pumps ◽  
Transcriptional Analysis ◽  
Systematic Analysis ◽  
Daily Lives ◽  
Single Strain ◽  
Content Type ◽  
Subinhibitory Concentrations ◽  
Different Strains

ABSTRACT Staphylococcus aureus-associated infections can be difficult to treat due to multidrug resistance. Thus, infection prevention is critical. Cationic antiseptics, such as chlorhexidine (CHX) and benzalkonium chloride (BKC), are liberally used in health care and community settings to prevent infection. However, increased administration of antiseptics has selected for S. aureus strains that show reduced susceptibilities to cationic antiseptics. This increased resistance has been associated with carriage of specific efflux pumps (QacA, QacC, and NorA). Since prior published studies focused on different strains and on strains carrying only a single efflux gene, the relative importance of these various systems to antiseptic resistance is difficult to ascertain. To overcome this, we engineered a collection of isogenic S. aureus strains that harbored norA, qacA, and qacC, individually or in combination. MIC assays showed that qacA was associated with increased resistance to CHX, cetrimide (CT), and BKC, qacC was associated with resistance to CT and BKC, and norA was necessary for basal-level resistance to the majority of tested antiseptics. When all three pumps were present in a single strain, an additive effect was observed in the MIC for CT. Transcriptional analysis revealed that expression of qacA and norA was significantly induced following exposure to BKC. Alarmingly, in a strain carrying qacA and norA, preexposure to BKC increased CHX tolerance. Overall, our results reveal increased antiseptic resistance in strains carrying multiple efflux pumps and indicate that preexposure to BKC, which is found in numerous daily-use products, can increase CHX tolerance. IMPORTANCE S. aureus remains a significant cause of disease within hospitals and communities. To reduce the burden of S. aureus infections, antiseptics are ubiquitously used in our daily lives. Furthermore, many antiseptic compounds are dual purpose and are found in household products. The increased abundance of antiseptic compounds has selected for S. aureus strains that carry efflux pumps that increase resistance to antiseptic compounds; however, the effect of carrying multiple pumps within S. aureus is unclear. We demonstrated that an isogenic strain carrying multiple efflux pumps had an additive resistance phenotype to cetrimide. Moreover, in a strain carrying qacA and norA, increased chlorhexidine tolerance was observed after the strain was preexposed to subinhibitory concentrations of a different common-use antiseptic. Taken together, our findings demonstrate cooperation between antiseptic resistance efflux pumps and suggest that their protective phenotype may be exacerbated by priming with subinhibitory concentrations of household antiseptics.

In vitro and in vivo inhibition of renin by fatty acids.

1978 ◽  
Vol 234 (6) ◽  
pp. E593 ◽  
Author(s):  
T A Kotchen ◽  
W J Welch ◽  
R T Talwalkar
Keyword(s):  
Blood Pressure ◽  
Fatty Acids ◽  
Linoleic Acid ◽  
Angiotensin Ii ◽  
Neutral Lipids ◽  
Pressor Response ◽  
Arterial Blood ◽  
Arachidonic Acids

Circulating neutral lipids inhibit the in vitro renin reaction. To identify the inhibitor(s), free fatty acids were added to human renin and homologous substrate. Capric, lauric, palmitoleic, linoleic, and arachidonic acids each inhibited the rate of angiotensin I production in vitro (P less than 0.01). Inhibition by polysaturated fatty acids (linoleic and arachidonic) was less (P less than 0.01) after catalytic hydrogenation of the double bonds. To evaluate an in vivo effect of renin inhibition intra-arterial blood pressure responses to infusions of renin and angiotensin II (5.0 microgram) were measured in anephric rats (n = 6) before and after infusion of linoleic acid (10 mg iv). Mean increase of blood pressure to angiotensin II before (75 mmHg +/- 9) and after (90 +/- 12) linoleic acid did not differ (P greater than 0.05). However, the pressor response to renin after linoleic acid (18 +/- 3) was less (P less than 0.00)) than that before (102 +/- 13). In summary, several fatty acids inhibit the in vitro renin reaction, and in part inhibition is dependent on unsaturation. Linoleic acid also inhibits the in vivo pressor response to renin. These results suggest that fatty acids may modify the measurement of plasma renin activity and may also affect angiotensin production in vivo.

scholarly journals Staphylococcus aureus Releases Proinflammatory Membrane Vesicles To Resist Antimicrobial Fatty Acids

mSphere ◽  
2020 ◽  
Vol 5 (5) ◽  
Author(s):  
Arnaud Kengmo Tchoupa ◽  
Andreas Peschel
Keyword(s):  
Fatty Acids ◽  
Staphylococcus Aureus ◽  
Immune Responses ◽  
Membrane Vesicle ◽  
Membrane Vesicles ◽  
Innate Immune ◽  
Toll Like Receptor ◽  
Content Type ◽  
Healthy Humans ◽  
Toll Like Receptor 2

ABSTRACT Staphylococcus aureus is a major pathogen, which colonizes one in three otherwise healthy humans. This significant spread of S. aureus is largely due to its ability to circumvent innate immune responses, including antimicrobial fatty acids (AFAs) on the skin and in nasal secretions. In response to AFAs, S. aureus swiftly induces resistance mechanisms, which have yet to be completely elucidated. Here, we identify membrane vesicle (MV) release as a resistance strategy used by S. aureus to sequester host-specific AFAs. MVs protect S. aureus against a wide array of AFAs. Strikingly, beside MV production, S. aureus modulates MV composition upon exposure to AFAs. MVs purified from bacteria grown in the presence of linoleic acid display a distinct protein content and are enriched in lipoproteins, which strongly activate Toll-like receptor 2 (TLR2). Cumulatively, our findings reveal the protective capacities of MVs against AFAs, which are counteracted by an increased TLR2-mediated innate immune response. IMPORTANCE The nares of one in three humans are colonized by Staphylococcus aureus. In these environments, and arguably on all mucosal surfaces, bacteria encounter fatty acids with antimicrobial properties. Our study uncovers that S. aureus releases membrane vesicles (MVs) that act as decoys to protect the bacterium against antimicrobial fatty acids (AFAs). The AFA-neutralizing effects of MVs were neither strain specific nor restricted to one particular AFA. Hence, MVs may represent “public goods” playing an overlooked role in shaping bacterial communities in AFA-rich environments such as the skin and nose. Intriguingly, in addition to MV biogenesis, S. aureus modulates MV composition in response to exposure to AFAs, including an increased release of lipoproteins. These MVs strongly stimulate the innate immunity via Toll-like receptor 2 (TLR2). TLR2-mediated inflammation, which helps to fight infections, may exacerbate inflammatory disorders like atopic dermatitis. Our study highlights intricate immune responses preventing infections from colonizing bacteria.

scholarly journals New MLSBResistance Geneerm(43) in Staphylococcus lentus

2012 ◽  
Vol 56 (9) ◽  
pp. 4746-4752 ◽  
Author(s):  
Sybille Schwendener ◽  
Vincent Perreten
Keyword(s):  
Staphylococcus Aureus ◽  
Resistance Gene ◽  
Regulatory Region ◽  
Dna Fragments ◽  
Content Type ◽  
Resistance Phenotype ◽  
Inducible Resistance

ABSTRACTThe search for a specific rRNA methylase motif led to the identification of the new macrolide, lincosamide, and streptogramin B resistance geneerm(43) inStaphylococcus lentus. An inducible resistance phenotype was demonstrated by cloning and expressingerm(43) and its regulatory region inStaphylococcus aureus. Theerm(43) gene was detected in two different DNA fragments, of 6,230 bp and 1,559 bp, that were each integrated at the same location in the chromosome in severalS. lentusisolates of human, dog, and chicken origin.

scholarly journals Contribution of Resistance-Nodulation-Division Efflux Pump OperonsmeU1-V-W-U2-Xto Multidrug Resistance of Stenotrophomonas maltophilia

2011 ◽  
Vol 55 (12) ◽  
pp. 5826-5833 ◽  
Author(s):  
Chao-Hsien Chen ◽  
Chiang-Ching Huang ◽  
Tsao-Chuen Chung ◽  
Rouh-Mei Hu ◽  
Yi-Wei Huang ◽  
...  
Keyword(s):  
Stenotrophomonas Maltophilia ◽  
Efflux Pump ◽  
Acquired Resistance ◽  
Type Systems ◽  
Resistant Mutant ◽  
Multidrug Resistant ◽  
Content Type ◽  
Membrane Fusion Protein ◽  
Resistance Nodulation Division

ABSTRACTKJ09C, a multidrug-resistant mutant ofStenotrophomonas maltophiliaKJ, was generated byin vitroselection with chloramphenicol. The multidrug-resistant phenotype of KJ09C was attributed to overexpression of a resistance nodulation division (RND)-type efflux system encoded by an operon consisting of five genes:smeU1,smeV,smeW,smeU2, andsmeX. Proteins encoded bysmeV,smeW, andsmeXwere similar to the membrane fusion protein, RND transporter, and outer membrane protein, respectively, of known RND-type systems. The proteins encoded bysmeU1andsmeU2were found to belong to the family of short-chain dehydrogenases/reductases. Mutant KJ09C exhibited increased resistance to chloramphenicol, quinolones, and tetracyclines and susceptibility to aminoglycosides; susceptibility to β-lactams and erythromycin was not affected. The expression of thesmeU1-V-W-U2-Xoperon was regulated by the divergently transcribed LysR-type regulator genesmeRv. Overexpression of the SmeVWX pump contributed to the acquired resistance to chloramphenicol, quinolones, and tetracyclines. Inactivation ofsmeVandsmeWcompletely abolished the activity of the SmeVWX pump, whereas inactivation ofsmeXalone decreased the activity of the SmeVWX pump. The enhanced aminoglycoside susceptibility observed in KJ09C resulted from SmeX overexpression.

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