Cloning and expression of Staphylococcus aureus plasmid-mediated quaternary ammonium resistance in Escherichia coli

Tennent, Jan M.; Lyon, B. R.; Gillespie, Matthew T.; May, John W.; Skurray, Ronald A.

doi:10.1128/aac.27.1.79

Cited by 120 publications

(72 citation statements)

References 15 publications

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“…Since the resistance of norA seems to be due to mutation in the transcriptional regulatory region that results in overexpression of norA mRNA Noguchi et al, 2002), it is difficult to clearly identify norA-mediated antiseptic resistance in S. aureus by detection of the resistance gene. In comparison, the qacA, qacB and smr genes have been found mainly on plasmids (Littlejohn et al, 1991;Lyon & Skurry, 1987;Tennent et al, 1985). Except for 7 bp, the sequence of qacB is identical to that of qacA, although their resistance profiles differ slightly (Littlejohn et al, 1991;Paulsen et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Susceptibilities to antiseptic agents and distribution of antiseptic-resistance genes qacA/B and smr of methicillin-resistant Staphylococcus aureus isolated in Asia during 1998 and 1999

Noguchi

Suwa

Narui

et al. 2005

Journal of Medical Microbiology

149

110

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Many antiseptic agents are used in hygienic handwashes in the prevention of nosocomial infections by methicillin-resistant Staphylococcus aureus (MRSA). The plasmid-borne genes qacA/B and smr confer resistance to cationic antiseptic agents in S. aureus. In this study, the susceptibilities for dyes and antiseptic agents (e.g. acriflavine, acrinol, benzalkonium chloride, benzethonium chloride, chlorhexidine digluconate and alkyldiaminoethylglycine hydrochloride) of 894 isolates of MRSA collected from 11 Asian countries (South Korea, China, the Philippines, Singapore, Vietnam, Thailand, Indonesia, India, Sri Lanka, Saudi Arabia and Japan) between 1998 and 1999 were examined. In addition, the distributions of the antiseptic-resistance genes qacA/B and smr were studied by PCR. Among the Asian MRSA isolates 57 . 7 % (516/894) were acriflavine-resistant. The smr gene was detected in 31 . 6 % (12/38) of MRSA isolates from India but only in 1 . 9 % (16/856) of all the isolates from other Asian countries. MRSA with qacA/B comprised 41 . 6 % (372/894) of the isolates across Asia. In addition, PFGE was performed to type the MRSA and grouped the tested 30 MRSA isolates with qacA/B into 21 PFGE types. The results indicated that qacA/B is functionally the most important gene mediating antiseptic resistance in the MRSA strains of Asia and that a specific MRSA with qacA/B was not prevalent in Asia but qacA/B were widely spread among MRSA of Asia, while the geographical distribution of smr is more limited.

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Section: Introductionmentioning

confidence: 99%

Susceptibilities to antiseptic agents and distribution of antiseptic-resistance genes qacA/B and smr of methicillin-resistant Staphylococcus aureus isolated in Asia during 1998 and 1999

Noguchi

Suwa

Narui

et al. 2005

Journal of Medical Microbiology

149

110

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“…The nearly identical S. aureus qacA and qacB MDR genes encode the first bacterial MDR transporters to be described (218), their discovery closely following that of mammalian Pglycoprotein. Investigation of the S. aureus QacA and QacB MFS pumps has been stimulated by the prevalence of qacA and qacB genes on multiresistance plasmids, such as pSK1, which are commonly isolated from clinical strains of this important human pathogen (88,160,219,220).…”

Section: Qacr Regulator Of S Aureus Qaca/b Mdr Genesmentioning

confidence: 99%

Regulation of Bacterial Drug Export Systems

Grkovic

Brown

Skurray

2002

Microbiol Mol Biol Rev

361

339

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The active transport of toxic compounds by membrane-bound efflux proteins is becoming an increasingly frequent mechanism by which cells exhibit resistance to therapeutic drugs. This review examines the regulation of bacterial drug efflux systems, which occurs primarily at the level of transcription. Investigations into these regulatory networks have yielded a substantial volume of information that has either not been forthcoming from or complements that obtained by analysis of the transport proteins themselves. Several local regulatory proteins, including the activator BmrR from Bacillus subtilis and the repressors QacR from Staphylococcus aureus and TetR and EmrR from Escherichia coli, have been shown to mediate increases in the expression of drug efflux genes by directly sensing the presence of the toxic substrates exported by their cognate pump. This ability to bind transporter substrates has permitted detailed structural information to be gathered on protein-antimicrobial agent-ligand interactions. In addition, bacterial multidrug efflux determinants are frequently controlled at a global level and may belong to stress response regulons such as E. coli mar, expression of which is controlled by the MarA and MarR proteins. However, many regulatory systems are ill-adapted for detecting the presence of toxic pump substrates and instead are likely to respond to alternative signals related to unidentified physiological roles of the transporter. Hence, in a number of important pathogens, regulatory mutations that result in drug transporter overexpression and concomitant elevated antimicrobial resistance are often observed

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“…A widespread mechanism to counteract the inhibitory action of such molecules is their secretion from the cell by membrane-bound multidrug resistance (MDR) transporters (Chopra & Roberts, 2001;Neyfakh et al, 1991;Tennent et al, 1985). For instance, the cationic berberine alkaloids produced by many plants are substrates for MDR pumps, such as QacA and NorA of Staphylococcus aureus (Hsieh et al, 1998;Neyfakh et al, 1993;Ng et al, 1994;Schumacher & Brennan, 2003).…”

Section: Introductionmentioning

confidence: 99%

LmrR-mediated gene regulation of multidrug resistance in Lactococcus lactis

et al. 2011

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Multidrug resistance (MDR) in Lactococcus lactis is due to the expression of the membrane ATP-binding cassette (ABC) transporter LmrCD. In the absence of drugs, the transcriptional regulator LmrR prevents expression of the lmrCD operon by binding to its operator site. Through an autoregulatory mechanism LmrR also suppresses its own expression. Although the lmrR and lmrCD genes have their own promoters, primer extension analysis showed the presence of a long transcript spanning the entire lmrR-lmrCD cluster, in addition to various shorter transcripts harbouring the lmrCD genes only. 'In-gel' Cu-phenanthroline footprinting analysis indicated an extensive interaction between LmrR and the lmrR promoter/operator region. Atomic force microscopy imaging of the binding of LmrR to the control region of lmrR DNA showed severe deformations indicative of DNA wrapping and looping, while LmrR binding to a fragment containing the lmrCD control region induced DNA bending. The results further suggest a drugdependent regulation mechanism in which the lmrCD genes are co-transcribed with lmrR as a polycistronic messenger. This leads to an LmrR-mediated regulation of lmrCD expression that is exerted from two different locations and by distinct regulatory mechanisms.

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Cloning and expression of Staphylococcus aureus plasmid-mediated quaternary ammonium resistance in Escherichia coli

Cited by 120 publications

References 15 publications

Susceptibilities to antiseptic agents and distribution of antiseptic-resistance genes qacA/B and smr of methicillin-resistant Staphylococcus aureus isolated in Asia during 1998 and 1999

Susceptibilities to antiseptic agents and distribution of antiseptic-resistance genes qacA/B and smr of methicillin-resistant Staphylococcus aureus isolated in Asia during 1998 and 1999

Regulation of Bacterial Drug Export Systems

LmrR-mediated gene regulation of multidrug resistance in Lactococcus lactis

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