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Gene Review

parE  -  DNA topoisomerase IV, subunit B

Escherichia coli str. K-12 substr. MG1655

Synonyms: ECK3021, JW2998, nfxD
 
 
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Disease relevance of parE

 

High impact information on parE

  • A topA mutation defective in topoisomerase I could be compensated by increasing both the parC and the parE gene dosage [6].
  • Mutants of this gene were isolated and showed the typical Par phenotype at nonpermissive temperature; thus the gene was named parE [6].
  • DNA sequence analysis of Escherichia coli parC and parE, encoding the subunits of topoisomerase IV (Topo IV) (Kato, J.-I., Suzuki, H., and Ikeda, H. (1992) J. Biol. Chem. 267, 25676-25684), showed that ParC was 22 amino acids longer on the N terminus and ParE was 29 amino acids longer on the C terminus than reported previously [2].
  • This parE mutation renders the encoded topo IV approximately 40-fold resistant to inhibition by novobiocin in vitro and imparts a similar resistance to inhibition of topo IV-mediated relaxation of supercoiled DNA in vivo [7].
  • This report is the first of a quinolone-resistant parE mutant and confirms the role of topoisomerase IV as a secondary target of norfloxacin in E. coli [1].
 

Chemical compound and disease context of parE

  • We searched for the mutations involved in high-level fluoroquinolone resistance (ciprofloxacin MIC > or = 8 microg/ml) of 11 clinical isolates of Escherichia coli. trans-Complementation tests with the wild-type gyrA and parC genes were positive for all strains whereas negative results were observed with the wild-type gyrB and parE genes [8].
 

Biological context of parE

  • The transduced strains KL16 and W3110parE10 were subsequently transformed with plasmids containing cloned parE from DH161 or KL16 [1].
  • The analogous region of parE was analyzed in 34 of 36 isolates by single-strand conformational polymorphism analysis and sequencing; however, no amino acid substitutions were discovered [9].
  • Overexpression of topoisomerase III at the nonpermissive temperature was shown subsequently to restore timely chromosome decatenation and suppress lethality in strains carrying either temperature-sensitive parE or parC alleles [10].
 

Associations of parE with chemical compounds

  • Cloned parE from DH161 increased norfloxacin resistance in the parE(Ts) background twofold at 30 degrees C and fourfold at 42 degrees C compared to those for cloned parE from KL16 [1].
  • In the presence of ampicillin, the resistance of a gyrA nfxD double mutant, DH161 nfxD gyrA (from EN226-3), was fully complemented by gyrA+ [11].
 

Other interactions of parE

  • It is suggested that the parC and parE genes code for the subunits of a new topoisomerase, named topo IV [6].
  • The region of the parE gene, homologous to the quinolone-resistant determining region of the gyrB gene, is not linked with the acquisition of quinolone resistance in Escherichia coli clinical isolates [12].
 

Analytical, diagnostic and therapeutic context of parE

References

  1. Quinolone resistance locus nfxD of Escherichia coli is a mutant allele of the parE gene encoding a subunit of topoisomerase IV. Breines, D.M., Ouabdesselam, S., Ng, E.Y., Tankovic, J., Shah, S., Soussy, C.J., Hooper, D.C. Antimicrob. Agents Chemother. (1997) [Pubmed]
  2. Escherichia coli topoisomerase IV. Purification, characterization, subunit structure, and subunit interactions. Peng, H., Marians, K.J. J. Biol. Chem. (1993) [Pubmed]
  3. Cloning and characterization of the parC and parE genes of Streptococcus pneumoniae encoding DNA topoisomerase IV: role in fluoroquinolone resistance. Pan, X.S., Fisher, L.M. J. Bacteriol. (1996) [Pubmed]
  4. Molecular characterization of the Salmonella typhimurium parE gene. Springer, A.L., Schmid, M.B. Nucleic Acids Res. (1993) [Pubmed]
  5. Requirement of topoisomerase IV parC and parE genes for cell cycle progression and developmental regulation in Caulobacter crescentus. Ward, D., Newton, A. Mol. Microbiol. (1997) [Pubmed]
  6. New topoisomerase essential for chromosome segregation in E. coli. Kato, J., Nishimura, Y., Imamura, R., Niki, H., Hiraga, S., Suzuki, H. Cell (1990) [Pubmed]
  7. Alteration of Escherichia coli topoisomerase IV to novobiocin resistance. Hardy, C.D., Cozzarelli, N.R. Antimicrob. Agents Chemother. (2003) [Pubmed]
  8. Analysis of the mutations involved in fluoroquinolone resistance of in vivo and in vitro mutants of Escherichia coli. Bachoual, R., Tankovic, J., Soussy, C.J. Microb. Drug Resist. (1998) [Pubmed]
  9. Contributions of individual mechanisms to fluoroquinolone resistance in 36 Escherichia coli strains isolated from humans and animals. Everett, M.J., Jin, Y.F., Ricci, V., Piddock, L.J. Antimicrob. Agents Chemother. (1996) [Pubmed]
  10. Topoisomerase III can serve as the cellular decatenase in Escherichia coli. Nurse, P., Levine, C., Hassing, H., Marians, K.J. J. Biol. Chem. (2003) [Pubmed]
  11. Limitations of plasmid complementation test for determination of quinolone resistance due to changes in the gyrase A protein and identification of conditional quinolone resistance locus. Soussy, C.J., Wolfson, J.S., Ng, E.Y., Hooper, D.C. Antimicrob. Agents Chemother. (1993) [Pubmed]
  12. The region of the parE gene, homologous to the quinolone-resistant determining region of the gyrB gene, is not linked with the acquisition of quinolone resistance in Escherichia coli clinical isolates. Ruiz, J., Casellas, S., Jimenez de Anta, M.T., Vila, J. J. Antimicrob. Chemother. (1997) [Pubmed]
  13. Molecular basis of quinolone resistance in Escherichia coli from wild birds. Jiménez Gómez, P.A., García de los Rios, J.E., Rojas Mendoza, A., de Pedro Ramonet, P., García Albiach, R., Reche Sainz, M.P. Can. J. Vet. Res. (2004) [Pubmed]
 
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