Ikeda Hideo, Shiraishi Kouya, Ogata Yasuyuki
Institute of Molecular Genetics, Medinet Inc, Tamagawadai 2-2-8, Setagaya-ku, Tokyo 158-0096, Japan.
Adv Biophys. 2004;38:3-20.
The frequency of illegitimate recombination has been measured by a lambda bio transducing phage assay during the induction of the E. coli lambda cI857 lysogen. Illegitimate recombination falls into two classes, short homology-independent and short homology-dependent illegitimate recombination. The former involves sequences with virtually no homology, and is mediated by DNA topoisomerases and controlled by the DNA binding protein HU. The latter is induced by UV irradiation or other DNA damaging agents and requires short regions of homology, usually contain 4 to 13 base pairs, at sites involved in recombination. It has been shown that the RecJ exonuclease promotes short homology-dependent illegitimate recombination, but that the RecQ helicase suppresses it. In addition, we have shown that the overexpression of RecE and RecT enhances the frequencies of spontaneous and UV-induced illegitimate recombination and that the RecJ, RecF, RecO, and RecR functions are required for this RecE-mediated illegitimate recombination. Moreover, we have also indicated that RecQ plays a role in the suppression of RecE-mediated illegitimate recombination, with the participation of DnaB, Fis, ExoI, and H-NS. Models have been proposed for these modes of recombination: the DNA gyrase subunit exchange model for short homology-independent illegitimate recombination and the "double-strand break and join" model for short homology-dependent illegitimate recombination. Many features of these models remain to be tested in future studies.
在大肠杆菌λcI857溶原菌诱导过程中,通过λbio转导噬菌体检测法测定了异常重组的频率。异常重组分为两类,即短同源性非依赖性和短同源性依赖性异常重组。前者涉及几乎没有同源性的序列,由DNA拓扑异构酶介导并受DNA结合蛋白HU控制。后者由紫外线照射或其他DNA损伤剂诱导,在参与重组的位点需要短的同源区域,通常包含4至13个碱基对。已经表明RecJ核酸外切酶促进短同源性依赖性异常重组,但RecQ解旋酶抑制它。此外,我们已经表明RecE和RecT的过表达会增加自发和紫外线诱导的异常重组频率,并且RecJ、RecF、RecO和RecR功能是这种RecE介导的异常重组所必需的。此外,我们还表明RecQ在抑制RecE介导的异常重组中起作用,涉及DnaB、Fis、ExoI和H-NS。已经为这些重组模式提出了模型:短同源性非依赖性异常重组的DNA促旋酶亚基交换模型和短同源性依赖性异常重组的“双链断裂并连接”模型。这些模型的许多特征仍有待未来研究进行检验。