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Tn7转座在转座子供体位点产生一个同源重组热点。

Tn7 transposition creates a hotspot for homologous recombination at the transposon donor site.

作者信息

Hagemann A T, Craig N L

机构信息

Department of Microbiology and Immunology, G. W. Hooper Foundation, University of California, San Francisco 94143.

出版信息

Genetics. 1993 Jan;133(1):9-16. doi: 10.1093/genetics/133.1.9.

Abstract

Homologous recombination at the bacterial transposon Tn7 donor site is stimulated 10-fold when Tn7 is activated to transpose at high frequency in RecD- Escherichia coli, where recombination is focused near the ends of double-chain breaks. This is observed as an increase in recombination between two lacZ heteroalleles when one copy of lacZ carries within it a Tn7 that is transposing at high frequency. This stimulation of recombination is dependent upon the presence of homology with the donor site, is independent of SOS induction, and is not due to a global stimulation of recombination. When stimulated by Tn7 transposition, the conversion events giving rise to Lac+ recombinants occur preferentially at the site of Tn7, suggesting that transposition is stimulating gene conversion at the donor site. These results support the model that Tn7 transposition occurs by a "cut and paste" mechanism, leaving a double-chain break at the donor site that is repaired by the host homologous recombination machinery; normally, repair would use homology in a sister chromosome to regenerate a copy of the transposon. This proposed series of events allows transposition that is nonreplicative, per se, to be effectively replicative.

摘要

当Tn7在RecD⁻大肠杆菌中被激活以高频转座时,细菌转座子Tn7供体位点的同源重组受到10倍的刺激,在这种情况下,重组集中在双链断裂的末端附近。当一个lacZ拷贝携带一个正在高频转座的Tn7时,在两个lacZ异源等位基因之间的重组增加就会观察到这种情况。这种重组刺激依赖于与供体位点的同源性存在,独立于SOS诱导,并且不是由于重组的全局刺激。当受到Tn7转座的刺激时,产生Lac⁺重组体的转换事件优先发生在Tn7的位点,这表明转座正在刺激供体位点的基因转换。这些结果支持这样的模型,即Tn7转座通过“剪切粘贴”机制发生,在供体位点留下双链断裂,由宿主同源重组机制修复;正常情况下,修复会利用姐妹染色单体中的同源性来再生转座子的一个拷贝。这一系列提出的事件使得本身非复制性的转座能够有效地进行复制。

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