Ogura T, Niki H, Mori H, Morita M, Hasegawa M, Ichinose C, Hiraga S
Department of Molecular Genetics, Kumamoto University Medical School, Japan.
J Bacteriol. 1990 Mar;172(3):1562-8. doi: 10.1128/jb.172.3.1562-1568.1990.
hopA mutants, which have been suggested to be defective in mini-F plasmid partitioning (H. Niki, C. Ichinose, T. Ogura, H. Mori, M. Morita, M. Hasegawa, N. Kusukawa, and S. Hiraga, J. Bacteriol. 170:5272-5278, 1988), were found to carry mutations in the gyrB gene, coding for the B subunit of DNA gyrase. In gyrB(HopA) mutants, relaxation of the superhelicity of plasmids, increased IncG incompatibility, and increased SopB protein production were observed. It is suggested that altered expression of the sop genes, which is due to relaxation of the mini-F plasmid DNA, causes both defective partitioning of the mini-F plasmids and increased IncG incompatibility in gyrB(HopA) mutants.
hopA突变体曾被认为在mini-F质粒分配方面存在缺陷(H. Niki、C. Ichinose、T. Ogura、H. Mori、M. Morita、M. Hasegawa、N. Kusukawa和S. Hiraga,《细菌学杂志》170:5272 - 5278,1988年),结果发现其gyrB基因发生了突变,该基因编码DNA促旋酶的B亚基。在gyrB(HopA)突变体中,观察到质粒超螺旋松弛、IncG不相容性增加以及SopB蛋白产量增加。有人提出,由于mini-F质粒DNA的松弛导致sop基因表达改变,从而导致gyrB(HopA)突变体中mini-F质粒分配缺陷和IncG不相容性增加。