The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
Gene Review

gyrB  -  DNA gyrase subunit B

Staphylococcus aureus RF122

 
 
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.
 

Disease relevance of gyrB

 

High impact information on gyrB

  • These findings demonstrate that DNA gyrase is the primary target and that topoisomerase IV is the secondary target for novobiocin and that the accumulation of point mutations in both the gyrB and the parE genes is associated with high-level resistance to novobiocin in S. aureus [1].
  • Species identification was confirmed by standard biochemical tests and analysis of 16S ribosomal DNA, gyrA, and gyrB sequences; all of the results were consistent with the S. aureus identification [3].
  • Second-step mutants selected with NSFQ-105 had gyrA(S84L) alterations; those obtained with sparfloxacin carried a gyrA(D83A) mutation or a novel gyrB deletion (DeltaRKSAL, residues 405 to 409) affecting a trypsin-sensitive region linking functional domains of S. aureus GyrB [4].
  • These results indicate that mutations in both gyrA and gyrB can be responsible for quinolone resistance in S. aureus [5].
  • No mutants had any changes in grlB, and only one had a mutation in gyrB giving rise to the novel substitution Asp-437-->His [6].
 

Biological context of gyrB

  • An expression plasmid was constructed by inserting the cloned genes into the Escherichia coli-S. aureus shuttle vector pAT19, and deletion plasmids carrying only functional gyrA and gyrB genes were derived from this plasmid [5].
  • This fast and simple protocol, applied to pure culture strains, was developed using the gyrB DNA sequence, as previously proposed by other authors [7].
 

Other interactions of gyrB

  • Portions of the gyrA (codons 60 to 120) and the gyrB (codons 420 to 480) genes of each clinical isolate were amplified by PCR and sequenced [8].
  • Only two gyrB mutants and one grlB mutant were observed among the isolates: all contained a previously unreported mutation [9].
  • No mutations were observed in either the gyrB or norA genes [10].

References

  1. Accumulation of mutations in both gyrB and parE genes is associated with high-level resistance to novobiocin in Staphylococcus aureus. Fujimoto-Nakamura, M., Ito, H., Oyamada, Y., Nishino, T., Yamagishi, J. Antimicrob. Agents Chemother. (2005) [Pubmed]
  2. Streptococcus pneumoniae DNA gyrase and topoisomerase IV: overexpression, purification, and differential inhibition by fluoroquinolones. Pan, X.S., Fisher, L.M. Antimicrob. Agents Chemother. (1999) [Pubmed]
  3. Vancomycin-resistant Staphylococcus aureus isolate from a patient in Pennsylvania. Tenover, F.C., Weigel, L.M., Appelbaum, P.C., McDougal, L.K., Chaitram, J., McAllister, S., Clark, N., Killgore, G., O'Hara, C.M., Jevitt, L., Patel, J.B., Bozdogan, B. Antimicrob. Agents Chemother. (2004) [Pubmed]
  4. Small-colony mutants of Staphylococcus aureus allow selection of gyrase-mediated resistance to dual-target fluoroquinolones. Pan, X.S., Hamlyn, P.J., Talens-Visconti, R., Alovero, F.L., Manzo, R.H., Fisher, L.M. Antimicrob. Agents Chemother. (2002) [Pubmed]
  5. Quinolone resistance mutations in the DNA gyrase gyrA and gyrB genes of Staphylococcus aureus. Ito, H., Yoshida, H., Bogaki-Shonai, M., Niga, T., Hattori, H., Nakamura, S. Antimicrob. Agents Chemother. (1994) [Pubmed]
  6. Selection of moxifloxacin-resistant Staphylococcus aureus compared with five other fluoroquinolones. Griggs, D.J., Marona, H., Piddock, L.J. J. Antimicrob. Chemother. (2003) [Pubmed]
  7. Bacillus cereus, Bacillus thuringiensis and Bacillus mycoides differentiation using a PCR-RE technique. Manzano, M., Cocolin, L., Cantoni, C., Comi, G. Int. J. Food Microbiol. (2003) [Pubmed]
  8. In vivo selection during pefloxacin therapy of a mutant of Staphylococcus aureus with two mechanisms of fluoroquinolone resistance. Tankovic, J., Desplaces, N., Duval, J., Courvalin, P. Antimicrob. Agents Chemother. (1994) [Pubmed]
  9. Characterization of gyrA, gyrB, grlA and grlB mutations in fluoroquinolone-resistant clinical isolates of Staphylococcus aureus. Takahashi, H., Kikuchi, T., Shoji, S., Fujimura, S., Lutfor, A.B., Tokue, Y., Nukiwa, T., Watanabe, A. J. Antimicrob. Chemother. (1998) [Pubmed]
  10. Mutations in the gyrA and grlA genes of quinolone-resistant clinical isolates of methicillin-resistant Staphylococcus aureus. Takahata, M., Yonezawa, M., Kurose, S., Futakuchi, N., Matsubara, N., Watanabe, Y., Narita, H. J. Antimicrob. Chemother. (1996) [Pubmed]
 
WikiGenes - Universities