Disease relevance of parC

• With E. coli, a gyrA, but not a parC, mutation raised the MIC of both compounds [1].
• Requirement of topoisomerase IV parC and parE genes for cell cycle progression and developmental regulation in Caulobacter crescentus [2].
• We determined a partial sequence of the Klebsiella pneumoniae parC gene, including the region analogous to the quinolone resistance-determining region of the Escherichia coli gyrA gene, and examined 26 clinical strains of K. pneumoniae for an association of alterations in GyrA and ParC with susceptibilities to quinolones [3].
• Fine mapping with phages from the collection of Kohara et al. is consistent with its being a parC allele [4].
• The topoisomerase IV subunit A gene, parC homolog, has been cloned and sequenced from Pseudomonas aeruginosa PAO1, with cDNA encoding the N-terminal region of Escherichia coli parC used as a probe [5].

High impact information on parC

• ParR protein binds cooperatively to the centromeric parC DNA region, thereby forming a complex that interacts with the filament-forming actin-like ParM protein in an ATP-dependent manner, suggesting that plasmid movement is powered by insertional polymerization of ParM [6].
• To understand further the role of the nucleoid and the min system in selection of the cell division site, we examined FtsZ localization in Escherichia coli cells lacking MinCDE and in parC mutants defective in chromosome segregation [7].
• Of 149 isolates, 102 (68.5%) had a MIC > or = 8 microg/mL, 138 (92.6%) had > or = 1 gyrA mutation, 101 (67.8%) had > or = 1 parC mutation, and 59 (39.6%) demonstrated OST [8].
• Furthermore, the fusion gene, parEC, complements the temperature-sensitive growth of both parC and parE strains, indicating that the ParEC protein can substitute for topoisomerase IV in vivo [9].
• DNA sequence analysis of DH161 revealed no changes in the topoisomerase IV parC quinolone resistance-determining region but did identify a single T-to-A mutation in parE at codon 445, leading to a change from Leu to His [10].

Chemical compound and disease context of parC

• Mutations in the parC region analogous to those in the quinolone resistance-determining region of gyrA were investigated in 27 clinical isolates of E. coli for which ciprofloxacin MICs were 0.0007 to 128 micrograms/ml [11].

Biological context of parC

• 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 [12].
• The centromere sequence parC of Escherichia coli low-copy-number plasmid R1 consists of two sets of 11 bp iterated sequences [13].
• The properties of the parC curvature agree with those of other curved DNA sequences. parC contains two regions of 5-fold repeated iterons separated by 39 bp [13].

Associations of parC with chemical compounds

• RESULTS: The dimer was lethal, in some cases exhibiting more activity than ciprofloxacin (particularly with wild-type cells and a parC mutant of S. aureus) [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 [14].
• Here we analysed the intrinsic sequence-directed curvature of parC by its migration anomaly in polyacrylamide gels [13].

Analytical, diagnostic and therapeutic context of parC

• For 11 mutants, minimum inhibitory concentrations (MICs) of antimicrobial agents were determined, and mutations in the region corresponding to the quinolone resistance-determining region (QRDR) of the Escherichia coli gyrA gene and the analogous region of the parC gene were analyzed [15].
• The molecular characterization of quinolone resistance was determinated by amplification of the gyrA and parC by PCR followed by sequencing of the respective amplicons [16].

References