Yamashita T, Hanada K, Iwasaki M, Yamaguchi H, Ikeda H
Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan.
J Bacteriol. 1999 Aug;181(15):4549-53. doi: 10.1128/JB.181.15.4549-4553.1999.
Illegitimate recombination that usually takes place at a low frequency is greatly enhanced by treatment with DNA-damaging agents. It is thought that DNA double-strand breaks induced by this DNA damage are important for initiation of illegitimate recombination. Here we show that illegitimate recombination is enhanced by overexpression of the DnaB protein in Escherichia coli. The recombination enhanced by DnaB overexpression occurred between short regions of homology. We propose a model for the initiation of illegitimate recombination in which DnaB overexpression may excessively unwind DNA at replication forks and induce double-strand breaks, resulting in illegitimate recombination. The defect in RecQ has a synergistic effect on the increased illegitimate recombination in cells containing the overproduced DnaB protein, implying that DnaB works in the same pathway as RecQ does but that they work at different steps.
通常以低频率发生的非法重组通过用DNA损伤剂处理而大大增强。据认为,这种DNA损伤诱导的DNA双链断裂对于非法重组的起始很重要。在这里,我们表明在大肠杆菌中DnaB蛋白的过表达增强了非法重组。由DnaB过表达增强的重组发生在同源性短区域之间。我们提出了一个非法重组起始的模型,其中DnaB过表达可能在复制叉处过度解开DNA并诱导双链断裂,从而导致非法重组。RecQ缺陷对含有过量产生的DnaB蛋白的细胞中增加的非法重组具有协同作用,这意味着DnaB与RecQ在相同的途径中起作用,但它们在不同的步骤起作用。