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大肠杆菌中紫外线抗性DNA复制的诱导:诱导稳定DNA复制作为一种SOS功能。

Induction of UV-resistant DNA replication in Escherichia coli: induced stable DNA replication as an SOS function.

作者信息

Kogoma T, Torrey T A, Connaughton M J

出版信息

Mol Gen Genet. 1979 Oct 2;176(1):1-9. doi: 10.1007/BF00334288.

Abstract

The striking similarity between the treatments that induce SOS functions and those that result in stable DNA replication (continuous DNA replication in the absence of protein synthesis) prompted us to examine the possibility of stable DNA replication being a recA+ lexA+-dependent SOS function. In addition to the treatments previously reported, ultraviolet (UV) irradiation or treatment with mitomycin C was also found to induce stable DNA replication. The thermal treatment of tif-1 strains did not result in detectable levels of stable DNA replication, but nalidixic acid readily induced the activity in these strains. The induction of stable DNA replication with malidixic acid was severely suppressed in tif-1 lexA mutant strains. The inhibitory activity of lexA3 was negated by the presence of the spr-51 mutation, an intragenic suppressor of lexA3. Induced stable DNA replication was found to be considerably more resistant to UV irradiation than normal replication both in a uvrA6 strain and a uvr+ strain. The UV-resistant replication occurred mostly in the semiconservative manner. The possible roles of stable DNA replication in repair of damaged DNA are discussed.

摘要

诱导SOS功能的处理方法与导致稳定DNA复制(在缺乏蛋白质合成的情况下持续进行DNA复制)的处理方法之间存在显著相似性,这促使我们研究稳定DNA复制是否是一种recA⁺ lexA⁺依赖性SOS功能。除了先前报道的处理方法外,还发现紫外线(UV)照射或丝裂霉素C处理也能诱导稳定DNA复制。对tif-1菌株进行热处理未导致可检测水平的稳定DNA复制,但萘啶酸很容易在这些菌株中诱导出该活性。在tif-1 lexA突变菌株中,萘啶酸诱导的稳定DNA复制受到严重抑制。spr-51突变(lexA3的基因内抑制子)的存在消除了lexA3的抑制活性。在uvrA6菌株和uvr⁺菌株中,发现诱导的稳定DNA复制比正常复制对紫外线照射的抗性要强得多。抗紫外线的复制大多以半保留方式进行。本文讨论了稳定DNA复制在受损DNA修复中的可能作用。

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