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首页> 外文期刊>Mutation Research: International Journal on Mutagenesis, Chromosome Breakage and Related Subjects >High and low UV-dose responses in SOS-induction of the precise excision of transposons tn1, Tn5 and Tn10 in Escherichia coli.
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High and low UV-dose responses in SOS-induction of the precise excision of transposons tn1, Tn5 and Tn10 in Escherichia coli.

机译：SOS诱导转座子tn1，Tn5和Tn10在大肠杆菌中的精确切除中的高剂量和低剂量UV反应。

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摘要

UV-inducible precise excision of transposons is a specific SOS-mutagenesis process. It deals with the deletion formation which has previously been demonstrated to involve direct or inverted IS-sequences of transposons. The process was used for revisiting the targeted and untargeted SOS-mutability and its relationship to the key genes for SOS-mutagenesis: the recA, lexA and umuDC. The precise excision of transposons Tn5 and Tn10 from the chromosomal insertion sites ade128 and cyc750 is induced in Escherichia coli K-12 and B cells, wild-type for DNA-repair, both by the low doses of UV-light ranging from 0.25 J m-2 to 2.5 J m-2 and the high doses within the range 5.0-40.0 J m-2. Precise excision of these transposons induced by the range of low doses incapable to induce targeted point mutations reveals its mostly untargeted nature. This process for the transposon Tn1 is not induced by UV-light within the range of doses 0.25-2.5 J m-2 while its induction is possible by UV-fluences ranging from 5.0 to 40.0 J m-2. A dose-response of the precise excision of Tn1 is similar to that of the UV-induced reversion of trpUAA point mutation that is targeted by nature and contrasts to the UV-inducible precise excision of Tn5 and Tn10. Both types of UV-inducible precise excision, demonstrated either by Tn1 or Tn5 and Tn10, are eliminated by mutations in the lexA, recA and umuDC genes indispensable for UV-induced SOS-mutability. The palindromic structures different for the transposons Tn1, Tn5 and Tn10 are discussed to be involved and affect the targeted and untargeted precise excision of transposons induced by UV-light. Copyright 1998 Elsevier Science B.V. All rights reserved.
机译：紫外线诱导的转座子的精确切除是一个特定的SOS诱变过程。它涉及缺失形成，该缺失形成先前已证明涉及转座子的直接或反向IS序列。该过程用于重新研究有针对性和无针对性的SOS变异性及其与SOS诱变关键基因的关系：recA，lexA和umuDC。在0.25 K m的低剂量紫外光照射下，大肠杆菌K-12和B细胞（DNA修复的野生型）可诱导从染色体插入位点ade128和cyc750精确去除转座子Tn5和Tn10。 -2至2.5 J m-2，高剂量在5.0-40.0 J m-2范围内。这些转座子的精确切除是由不能诱导靶点突变的低剂量范围引起的，揭示了它的大部分是非靶向性质。在剂量0.25-2.5 J m-2的范围内，紫外线不会诱导转座子Tn1的这一过程，而在5.0至40.0 J m-2的UV通量下，它的诱导是可能的。 Tn1精确切除的剂量反应类似于自然界靶向的UV诱导的trpUAA点突变回复，与紫外线诱导的Tn5和Tn10精确切除形成对比。通过Tn1或Tn5和Tn10证明的两种类型的紫外线诱导精确切除都可以通过lexA，recA和umuDC基因中的突变消除，而lexA，recA和umuDC基因是紫外线诱导的SOS突变所必需的。讨论了转座子Tn1，Tn5和Tn10的回文结构不同，这些结构涉及并影响有针对性的和无目标的由紫外线诱导的转座子的精确切除。版权所有1998 Elsevier Science B.V.保留所有权利。

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