ArticleAntimicrobial agents and chemotherapy2000
Cloning and nucleotide sequence of the DNA gyrase (gyrA) gene from Mycoplasma hominis and characterization of quinolone-resistant mutants selected in vitro with trovafloxacin.
Article in Antimicrobial agents and chemotherapy, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 30 citations in OpenAlex.
- Comparative Genomic Analysis of Multi-Drug ResistantMicroorganisms · 2023Article
- Phenotypic Antimicrobial Susceptibility and Genotypic Characterization of ClinicalFrontiers in microbiology · 2021Article
- The Expanding Role of Pyridine and Dihydropyridine Scaffolds in Drug Design.Drug design, development and therapy · 2021Review
- Mycoplasma genitalium Antimicrobial Resistance in Community and Sexual Health Clinic Patients, Auckland, New Zealand.Emerging infectious diseases · 2020Article
- Synthesis and biological evaluation of 3-(1,3,4-oxadiazol-2-yl)-1,8-naphthyridin-4(1MedChemComm · 2018Article
- Suppression of gyrase-mediated resistance by C7 aryl fluoroquinolones.Nucleic acids research · 2016Article
- Alterations in the Quinolone Resistance-Determining Regions and Fluoroquinolone Resistance in Clinical Isolates and Laboratory-Derived Mutants of Mycoplasma bovis: Not All Genotypes May Be Equal.Applied and environmental microbiology · 2016Article
- DNA Gyrase Is the Target for the Quinolone Drug Ciprofloxacin in Arabidopsis thaliana.The Journal of biological chemistry · 2016Article
- Molecular mechanism of fluoroquinolones resistance in Mycoplasma hominis clinical isolates.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2014Article
- Contribution of topoisomerase IV mutation to quinolone resistance in Mycoplasma genitalium.Antimicrobial agents and chemotherapy · 2013Article
- Revised minimal standards for description of new species of the class Mollicutes (division Tenericutes).International journal of systematic and evolutionary microbiology · 2007Article
- Mutation rate and evolution of fluoroquinolone resistance in Escherichia coli isolates from patients with urinary tract infections.Antimicrobial agents and chemotherapy · 2003Article
- Mutations in 23S rRNA account for intrinsic resistance to macrolides in Mycoplasma hominis and Mycoplasma fermentans and for acquired resistance to macrolides in M. hominis.Antimicrobial agents and chemotherapy · 2002Article
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6 authors at 1 institution in 1 country.
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Abstract
We report the cloning and characterization of the gyrA gene of the Mycoplasma hominis DNA gyrase, which was previously shown to be associated with quinolone resistance in this organism. The 2,733-bp gyrA gene encodes a protein of 911 amino acids with a calculated molecular mass of 102.5 kDa. As expected, M. hominis GyrA exhibits higher homology with the GyrA subunits of the gram-positive bacteria Clostridium acetobutylicum, Bacillus subtilis, Streptococcus pneumoniae, and Staphylococcus aureus than with its Escherichia coli counterpart. Knowing the entire sequence of the gyrA gene of M. hominis could be very useful for confirming the role of the GyrA subunit in fluoroquinolone resistance. Twenty-nine mutants of M. hominis were selected stepwise for resistance to trovafloxacin, a new potent fluoroquinolone, and their gyrA, gyrB, parC, and parE quinolone resistance-determining regions were characterized. Three rounds of selection yielded 3 first-step, 12 second-step, and 14 third-step mutants. The first-step mutants harbored a single substitution, Glu460-->Lys (E. coli coordinates), in ParE. GyrA changes, Ser83-->Leu, Glu87-->Lys, and Ala119-->Glu or Val, were found only in the second round of selection. At the third step, additional substitutions, at ParC Ser80, Ser81, and Glu84 and ParE Leu440, associated with high-level resistance to fluoroquinolones, appeared. Thus, high-level resistance to trovafloxacin required three steps and was associated with alterations in both fluoroquinolone targets. According to these genetic data, in M. hominis, as in Staphylococcus aureus and Streptococcus pneumoniae, topoisomerase IV seems to be the primary target of trovafloxacin.
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