known as topoisomerase poisons. By binding to the enzyme they trap it in a transient step of the catalytic cycle, preventing the reunion of a G-segment. This results in an accumulation of double-strand breaks, stalling of replication forks and cell death. Quinolone-resistant bacteria frequently harbor mutated topoisomerases that resist quinolone binding. The subunit A is selectively inactivated by antibiotics such as oxolinic and nalidixic acids. The subunit B is selectively inactivated by antibiotics such as coumermycin A1 and novobiocin. Inhibition of either subunit blocks supertwisting activity. Phage T4 Phage T4 genes 39, 52 and 60 encode proteins that form a DNA gyrase that is employed in phage DNA replication during infection of the E. coli bacterial host. The phage gene 52 protein shares homology with the bacterial gyrase gyrA subunit and the phage gene 39 protein shares homology with the gyrB subunit. Since the host E. coli DNA gyrase can partially compensate for the loss of the phage gene products, mutants defective in either genes 39, 52 or 60 do not completely abolish phage DNA replication, but rather delay its initiation. Mutants defective in genes 39, 52 or 60 show increased genetic recombination as well as increased base-substitution and deletion mutation suggesting that the host compensated DNA synthesis is less accurate than that directed by wild-type phage. A mutant defective in gene 39 also shows increased sensitivity to inactivation by ultraviolet irradiation during the stage of phage infection after initiation of DNA replication when multiple copies of the phage chromosome are present. See also GyrA RNA motif References External links PDBe-KB : an overview of all the structure information available in the PDB for Escherichia coli DNA gyrase subunit A PDBe-KB : an overview of all the structure information available in the PDB for Salmonella enterica DNA gyrase subunit B DNA EC 5.99.1