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Related Concept Videos

Inhibitors of Bacterial DNA Synthesis01:28

Inhibitors of Bacterial DNA Synthesis

Bacterial pathogens depend on precise and efficient DNA replication to sustain infection. Two type II topoisomerases—DNA gyrase and topoisomerase IV—are critical to this process, as they resolve DNA supercoiling and unlink chromosomes during replication. Fluoroquinolones, synthetic derivatives of quinolones, exploit this mechanism by stabilizing the transient DNA–enzyme cleavage complex, preventing strand religation, and causing lethal double-strand breaks. These antibiotics are selectively...
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Antibiotic resistance in bacteria arises when microorganisms evolve the ability to withstand drugs designed to kill them or inhibit their growth, rendering once-effective treatments useless. This phenomenon, driven by genetic change and selection under antibiotic exposure, poses a profound threat to modern medicine. Mechanisms include drug-inactivating enzymes (e.g., β-lactamases), efflux pumps that eject antibiotics, mutations altering antibiotic targets, decreased drug uptake, and acquisition...
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Quorum sensing is a mechanism of bacterial communication that enables coordinated gene expression in response to changes in population density. This facilitates collective behaviors that enhance survival, resource acquisition, and ecological adaptation. This process relies on small signaling molecules called autoinducers that accumulate as bacterial populations grow. When a critical threshold concentration of autoinducers is reached, bacterial cells collectively modify gene expression,...
Plasmids01:28

Plasmids

Plasmids are extrachromosomal DNA molecules found in bacteria, archaea, and some eukaryotic microbes like yeast. These small, circular DNA structures typically contain fewer than 30 genes, although some may exist linearly. Plasmids vary in their number within a cell, known as copy number. Single-copy plasmids are present in one copy per cell and multi-copy plasmids are present in multiple copies, reaching over 100 copies per cell.Plasmids usually replicate independently of the chromosomal DNA...
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Methicillin-resistant Staphylococcus aureus (MRSA) presents a critical public health threat, arising from its capacity to resist β-lactam antibiotics due to acquisition of the mecA gene within the staphylococcal cassette chromosome mec (SCCmec). This gene encodes penicillin-binding protein 2a (PBP2a), which impairs binding efficacy of methicillin and other β-lactams. MRSA has evolved into distinct clonal lineages impacting humans and animals alike, reinforcing its significance within the One...
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Related Experiment Video

Updated: Jul 8, 2026

Quantification of Violacein in Chromobacterium violaceum and Its Inhibition by Bioactive Compounds
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Is plasmid-mediated quinolone resistance a clinically significant problem?

L Poirel, V Cattoir, P Nordmann

    Clinical Microbiology and Infection : the Official Publication of the European Society of Clinical Microbiology and Infectious Diseases
    |January 15, 2008
    PubMed
    Summary

    Plasmid-mediated quinolone resistance (PMQR) mechanisms like Qnr, AAC(6')-Ib-cr, and QepA are emerging in Enterobacteriaceae. These low-level resistance factors may promote the development of higher-level chromosomal resistance.

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    Area of Science:

    • Microbiology
    • Molecular Biology
    • Genetics

    Background:

    • Enterobacteriaceae commonly exhibit chromosomal quinolone resistance.
    • Plasmid-mediated quinolone resistance (PMQR) is an emerging concern.
    • Known PMQR mechanisms include Qnr proteins, AAC(6 ext{ extprime}) -Ib-cr, and QepA efflux pumps.

    Discussion:

    • Qnr proteins inhibit quinolone action by protecting DNA gyrase and topoisomerase IV.
    • AAC(6 ')-Ib-cr acetylates fluoroquinolones like norfloxacin and ciprofloxacin.
    • QepA facilitates the extrusion of hydrophilic fluoroquinolones via an efflux pump mechanism.

    Key Insights:

    • PMQR determinants confer low-level resistance to quinolones and fluoroquinolones.
    • These low-level resistance mechanisms can act as a predisposing factor.
    • Facilitates the selection and emergence of additional chromosomally-encoded resistance mechanisms.

    Outlook:

    • Understanding PMQR is crucial for developing effective antimicrobial strategies.
    • Monitoring the spread of PMQR is essential to combat rising antibiotic resistance.
    • Further research into novel therapeutic targets to overcome PMQR is warranted.