Travers A, Schneider R, Muskhelishvili G
MRC Laboratory of Molecular Biology, Hills Road, Cambridge CB2 2QH, UK.
Biochimie. 2001 Feb;83(2):213-7. doi: 10.1016/s0300-9084(00)01217-7.
The nucleoid-associated protein FIS modulates the topology of DNA in a growth-phase dependent manner functioning homeostatically to counteract excessive levels of negative superhelicity. We propose that this is achieved by at least two mechanisms: the physical constraint of low levels of negative superhelicity by FIS binding to DNA and by a reduction in the expression and effectiveness of DNA gyrase. In addition, high levels of expression of the fis gene do themselves require a high negative superhelical density. On DNA substrates containing phased high affinity binding sites, as exemplified by the upstream activating sequence of the tyrT promoter, FIS forms tightly bent DNA structures, or microloops, that are necessary for the optimal expression of the promoter. We suggest that these microloops compensate in part for the FIS-induced lowering of the superhelical density.
类核相关蛋白FIS以生长阶段依赖性方式调节DNA拓扑结构，起到稳态作用以抵消过高水平的负超螺旋。我们认为这至少通过两种机制实现：FIS与DNA结合对低水平负超螺旋的物理限制，以及DNA回旋酶表达和活性的降低。此外，fis基因的高表达本身确实需要高负超螺旋密度。在含有阶段性高亲和力结合位点的DNA底物上，如tyrT启动子的上游激活序列所示，FIS形成紧密弯曲的DNA结构或微环，这是启动子最佳表达所必需的。我们认为这些微环部分补偿了FIS诱导的超螺旋密度降低。
