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首页> 美国卫生研究院文献>Journal of Bacteriology >Involvement of integration host factor (IHF) in maintenance of plasmid pSC101 in Escherichia coli: mutations in the topA gene allow pSC101 replication in the absence of IHF.
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Involvement of integration host factor (IHF) in maintenance of plasmid pSC101 in Escherichia coli: mutations in the topA gene allow pSC101 replication in the absence of IHF.

机译：整合宿主因子（IHF）参与大肠杆菌中质粒pSC101的维持：topA基因突变允许在没有IHF的情况下复制pSC101。

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摘要

Integration host factor (IHF), encoded by the himA and himD genes, is a histonelike DNA-binding protein that participates in many cellular functions in Escherichia coli, including the maintenance of plasmid pSC101. We have isolated and characterized a chromosomal mutation that compensates for the absence of IHF and allows the maintenance of wild-type pSC101 in him mutants, but does not restore IHF production. The mutation is recessive and was found to affect the gene topA, which encodes topoisomerase I, a protein that relaxes negatively supercoiled DNA and acts in concert with DNA gyrase to regulate levels of DNA supercoiling. A previously characterized topA mutation, topA10, could also compensate for the absence of IHF to allow pSC101 replication. IHF-compensating mutations affecting topA resulted in a large reduction in topoisomerase I activity, and plasmid DNA isolated from such strains was more negatively supercoiled than DNA from wild-type strains. In addition, our experiments show that both pSC101 and pBR322 plasmid DNAs isolated from him mutants were of lower superhelical density than DNA isolated from Him+ strains. A concurrent gyrB gene mutation, which reduces supercoiling, reversed the ability of topA mutations to compensate for a lack of him gene function. Together, these findings indicate that the topological state of the pSC101 plasmid profoundly influences its ability to be maintained in populations of dividing cells and suggest a model to account for the functional interactions of the him, rep, topA, and gyr gene products in pSC101 maintenance.
机译：由himA和himD基因编码的整合宿主因子（IHF）是一种组蛋白样DNA结合蛋白，它参与大肠杆菌的许多细胞功能，包括质粒pSC101的维持。我们已经分离并鉴定了一种染色体突变，该突变弥补了IHF的缺失，并允许在他的突变体中维持野生型pSC101，但不能恢复IHF的产生。该突变是隐性的，发现影响基因topA，该基因编码拓扑异构酶I，该蛋白使负超螺旋DNA松弛，并与DNA促旋酶协同作用，调节DNA超螺旋的水平。先前表征的topA突变topA10也可以弥补IHF的缺失，从而允许pSC101复制。影响topA的IHF补偿性突变导致拓扑异构酶I活性大大降低，并且从此类菌株中分离的质粒DNA比野生型菌株中的DNA更负超螺旋。此外，我们的实验表明，从hes突变体分离的pSC101和pBR322质粒DNA的超螺旋密度均低于从Him +菌株分离的DNA。并发的gyrB基因突变减少了超螺旋，逆转了topA突变弥补he基因功能缺失的能力。总之，这些发现表明，pSC101质粒的拓扑状态深刻影响了其在分裂细胞群体中维持的能力，并提出了一个模型来说明在pSC101维持过程中him，rep，topA和gyr基因产物的功能相互作用。 。

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