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首页> 外文期刊>Journal of bacteriology >Mitomycin-induced lethality of Escherichia coli cells containing the ColE1 Plasmid: involvement of the kil gene.
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Mitomycin-induced lethality of Escherichia coli cells containing the ColE1 Plasmid: involvement of the kil gene.

机译：丝裂霉素诱导的含有ColE1质粒的大肠杆菌细胞的致死性：涉及kil基因。

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Escherichia coli cells containing the ColE1 plasmid or related plasmids are killed by considerably lower levels of mitomycin C (MTC) than are plasmid-free cells. Since exposure to MTC induces high levels of synthesis of the plasmid-encoded colicin toxin, it was originally thought that the killing effect was due to the increased levels of colicin. This possibility was discounted when it was shown that deletion mutations in the plasmid lacking most of the colicin (cea) gene still sensitized host cells to MTC. Only when the region containing the cea gene promoter was deleted did the killing effect disappear. This led to the suggestion that transcription originating from the cea gene promoter and not the colicin protein itself was required for killing. Transcription-blocking mutations in the cea gene support this suggestion. It was proposed that there is a gene (kil) located downstream from the cea gene in the same operon that is responsible for MTC killing and colicin transport. The precise location of the kil gene in ColE1 can be predicted by piecing together published sequence information. We used available sequence data to construct a number of well-defined plasmid mutants to further examine the relevance of transcription from the cea promoter and the kil gene to drug-induced killing and colicin transport. The most informative mutant had a small insertion in the kil gene. This mutant behaved as predicted; cells containing it had a greatly lowered sensitivity to MTC and were severely inhibited in the transport of colicin.
机译：与无质粒细胞相比，含有ColE1质粒或相关质粒的大肠杆菌细胞被丝裂霉素C（MTC）的水平要低得多。由于暴露于MTC会诱导质粒编码的大肠菌素毒素的高水平合成，因此最初认为杀伤作用是由于大肠菌素水平的提高。当发现缺少大多数大肠菌素（cea）基因的质粒中的缺失突变仍然使宿主细胞对MTC敏感时，这种可能性就被忽略了。只有当含有cea基因启动子的区域被删除时，杀伤作用才消失。这导致了暗示，杀死是需要从cea基因启动子而不是大肠菌素蛋白本身开始的转录。 cea基因中的转录阻断突变支持这一建议。有人提出，在同一操纵子中，cea基因的下游有一个基因（kil），负责杀死MTC和大肠菌素。通过将公开的序列信息拼凑在一起，可以预测kil基因在ColE1中的精确位置。我们使用可用的序列数据来构建许多定义明确的质粒突变体，以进一步检查从cea启动子和kil基因转录与药物诱导的杀伤和大肠菌素运输的相关性。信息最丰富的突变体在kil基因中插入很小。该突变体表现出预期。含有它的细胞对MTC的敏感性大大降低，并在大肠菌素的运输中受到严重抑制。

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