Repression of cointegration ability of insertion element IS1 by transcriptional readthrough from flanking regions
Repression of cointegration ability of insertion element IS1 by transcriptional readthrough from flanking regions
复制标题
通过侧翼区域的转录通读抑制插入元件 IS1 的共整合能力
DOI：
10.1016/0092-8674(83)90143-5
复制
发表时间：
1983
期刊：
影响因子：
64.5
通讯作者：
E. Ohtsubo
中科院分区：
文献类型：
--
作者：
C. Machida;Y. Machida;Hwa;K. Ishizaki;E. Ohtsubo
我们描述了一种抑制机制，其中从基因转录到IS1序列的读出信息抑制了其介导质粒协整的能力。这一机制源于以下研究：去除Tn9转座子中氯霉素耐药基因的启动子区域，或在氯霉素耐药基因下游噬菌体17引入一个强转录终止子，可以增加下游IS1序列在特定方向上的协整能力。在氯霉素抗性基因下游与上述IS1序列方向相反的IS1序列的协整能力也可以被抑制。体外合成的转录本分析表明，氯霉素耐药基因的转录本在两个方向上都被读取到位于基因下游的IS1序列。这种类型的抑制可能是控制IS1元件转位率的一种机制，而IS1元件显然不编码抑制因子的结构基因。
We describe a repression mechanism in which readthrough messages transcribed from a gene into an IS1 sequence inhibit its ability to mediate plasmid cointegration. This mechanism was derived from the demonstration that removal of the promoter region of the chloramphenicol resistance gene in transposon Tn9, or introduction of a strong transcription terminator of phage l7 downstream of the chloramphenicol resistance gene, increases the cointegration ability of the downstream IS1 seguence when in a particular orientation. The cointegration ability of an IS1 sequence downstream of the chloramphenicol resistance gene but in an orientation opposite that of the above-mentioned IS1 sequence also can be repressed. Analysis of transcripts synthesized in vitro showed that the transcripts of the chloramphenicol resistance gene were read through into the IS1 sequence located downstream of the gene in either orientation. Repression of this type may be one mechanism that controls the rate of transposition of the IS1 element, which apparently does not encode a structural gene for repressor.