Disease relevance of gyrA

• With E. coli, a gyrA, but not a parC, mutation raised the MIC of both compounds [1].
• A nucleotide mutation associated with fluoroquinolone resistance observed in gyrA of in vitro obtained Rhodococcus equi mutants [2].
• Cloning the gyrA gene of Bacillus subtilis [3].
• Cloning and sequence analysis of gyrA gene of Klebsiella pneumoniae [4].
• To study the mechanism of DNA gyrase-mediated illegitimate recombination in Escherichia coli, we isolated temperature-sensitive gyrA mutants that confer spontaneous illegitimate recombination and spontaneous induction of lambda prophage at higher frequencies than that in the wild-type [5].

High impact information on gyrA

• In the Deltafis strain, both topA and gyrA/B genes were found to be upregulated [6].
• Forward mutation frequencies and rates were measured at two chromosomal loci, rpoB and gyrA, and base substitution and frameshift mutation frequencies were measured on an F'(lacZ) episome [7].
• When wild-type Pol II (polB+) was replaced on the chromosome by a proofreading-defective Pol II exo- (polBex1), there was a significant increase in mutation frequencies to rifampicin resistance (RifR) (rpoB) and nalidixic acid resistance (NalR) (gyrA) [7].
• In this paper we report a deletion analysis of the gyrA and gyrB promoter regions [8].
• Multicopy recombinant plasmids containing the Escherichia coli gyrA gene are able to complement both the growth defects and the elevated his operon expression associated with the hisW mutations [9].

Chemical compound and disease context of gyrA

• The Bacillus wild type gyrA gene, which confers sensitivity to nalidixic acid, is dominant in E. coli as is the E. coli gene [3].
• Complementation of possible DNA gyrase mutations with a plasmid-borne, wild-type Escherichia coli gyrA gene indicated that altered DNA gyrase was at least partly responsible for ciprofloxacin resistance in all strains tested [10].
• In vivo selection of reduced enrofloxacin susceptibility in Ornithobacterium rhinotracheale and its resistance-related mutations in gyrA [11].
• Auxotrophic phenotypes of Escherichia coli and Salmonella typhimurium mesophilic parents were demonstrated by these mutants if they were cultivated on minimal agar with cellobiose at 48 degrees C or 54 degrees C or on a minimal agar with glucose at 37 degrees C. The T48 alleles mapped in the gyrA region of E. coli or S. typhimurium chromosome [12].
• Antibacterial activities of gatifloxacin (AM1155), a new C-8-methoxy fluoroquinolone, and two structurally related compounds, AM1121 and ciprofloxacin, were studied with an isogenic set of ten quinolone-resistant, gyrA (gyrase) mutants of Escherichia coli [13].

Biological context of gyrA

• Typhimurium representative single-step mutants showed reduced susceptibilities associated with point mutations in the QRDR of the gyrA gene or efflux pump system [14].
• The molecular background for the fluoroquinolone-resistance was investigated and point mutations in gyrA and parC leading to amino-acid substitutions in quinolone-resistance determining regions of GyrA and ParC were demonstrated [15].
• The gene gyrA encoding the DNA gyrase A subunit of Klebsiella pneumoniae has been cloned in the plasmid pBR322 [4].
• The cloned DNA precisely defines the physical location of the gyrA mutation on the B. subtilis chromosome [3].
• This T4 topoisomerase subunit shares significant amino acid sequence homology with the gyrA subunit of bacterial gyrases and the carboxyl-half of yeast topoisomerase II in spite of the large differences in their sizes, confirming their functional equivalence in type II enzyme directed DNA topoisomerization [16].

Anatomical context of gyrA

• Development of a rapid assay for detecting gyrA mutations in Escherichia coli and determination of incidence of gyrA mutations in clinical strains isolated from patients with complicated urinary tract infections [17].

Associations of gyrA with chemical compounds

• With S. aureus, the dimer selected spontaneous resistant gyrA mutants, whereas ciprofloxacin selected a parC mutant [1].
• The objective of this study was to analyse an array of ciprofloxacin and norfloxacin derivatives in order to determine those with good activity against bacteria that already present fluoroquinolone resistance associated with mutations in the gyrA and/or parC genes [18].
• The stimulation is abolished by coumermycin A1 and is not found in extracts of nalidixic acid-resistant (gyrA) mutants [19].
• Stimulation of gyrA expression in an in vitro transcription-translation system by novobiocin, a DNA gyrase inhibitor, depends on the DNA concentration in the extract [20].
• Six nalidixic acid-resistant isolates of C. jejuni were shown to carry mutations in gyrA [21].

Other interactions of gyrA

• We characterized gyrA and parC mutations and organic solvent tolerance (OST) [22].
• In this study, the quinolone resistance-determining region (QRDR) in gyrA and gyrB of in vitro fluoroquinolone-resistant Rhodococcus equi mutants was sequenced [2].
• Conjugation experiments established the following gene order: gyrA (formerly nalA) lysP metG his [23].

Analytical, diagnostic and therapeutic context of gyrA

• Intragenic gyrA fragments of 668 and 2,500 bp from strain Q2 were amplified by the polymerase chain reaction [24].
• Drug-resistant strains of Escherichia coli were selected by serial passage in the presence of ofloxacin, and a mutation was mapped near the gyrA gene of DNA gyrase [25].
• In the first, increasing amounts of wild-type gyrA allele moderately increased minimum inhibitory concentrations to quinolone antibiotics [26].
• This resulted in alpha arteether resistant and nalidixic acid sensitive phenotype clearly demonstrating the use of gyrA mutant strains in differentiating alpha and beta isomers of arteether by this simple bioassay [27].
• Molecular cloning of the gyrA and gyrB genes of Bacteroides fragilis encoding DNA gyrase [28].

References