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J. Biol. Chem., Vol. 275, Issue 44, 34780-34786, November 3, 2000
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and
From the Department of Pharmacology, University of Minnesota
Medical School, Minneapolis, Minnesota 55455
The ability of DNA gyrase (Gyr) to wrap the DNA
strand around itself allows Gyr to introduce negative supercoils into
DNA molecules. It has been demonstrated that the deletion of the
C-terminal DNA-binding domain of the GyrA subunit abolishes the ability
of Gyr to wrap the DNA strand and catalyze the supercoiling reaction (Kampranis, S. C., and Maxwell, A. (1996) Proc. Natl. Acad.
Sci. U. S. A. 93, 14416-14421). By using this mutant Gyr, Gyr
(A59), we have studied effects of Gyr-mediated wrapping of the DNA
strand on its replicative function and its interaction with the
quinolone antibacterial drugs. We find that Gyr (A59) can
support oriC DNA replication in vitro. However,
Gyr (A59)-catalyzed decatenation activity is not efficient enough to
complete the decatenation of replicating daughter DNA molecules. As is
the case with topoisomerase IV, the active cleavage and reunion
activity of Gyr is required for the formation of the ternary complex
that can arrest replication fork progression in vitro.
Although the quinolone drugs stimulate the covalent Gyr (A59)-DNA
complex formation, the Gyr (A59)-quinolone-DNA ternary complexes do not
arrest the progression of replication forks. Thus, the
quinolone-induced covalent topoisomerase-DNA complex formation is
necessary but not sufficient to cause the inhibition of DNA
replication. We also assess the stability of ternary complexes formed
with Gyr (A59), the wild type Gyr, or topoisomerase IV. The ternary
complexes formed with Gyr (A59) are more sensitive to salt than those
formed with either the wild type Gyr or topoisomerase IV. Furthermore,
a competition experiment demonstrates that the ternary complexes formed
with Gyr (A59) readily disassociate from the DNA, whereas the ternary
complexes formed with either the wild type Gyr or topoisomerase IV
remain stably bound. Thus, Gyr-mediated wrapping of the DNA strand is required for the formation of the stable Gyr-quinolone-DNA ternary complex that can arrest replication fork progression.
Member of the University of Minnesota Comprehensive Cancer Center.
To whom correspondence should be addressed: 6-120 Jackson Hall, 321 Church St. SE, Minneapolis, MN 55455. Tel.: 612-626-3101; Fax:
612-625-8408; E-mail: hiasa001@tc.umn.edu.
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