Suppr超能文献

recO和recR突变会延迟大肠杆菌中SOS反应的诱导。

recO and recR mutations delay induction of the SOS response in Escherichia coli.

作者信息

Hegde S, Sandler S J, Clark A J, Madiraju M V

机构信息

Department of Microbiology, University of Texas Health Center, Tyler 75710.

出版信息

Mol Gen Genet. 1995 Jan 20;246(2):254-8. doi: 10.1007/BF00294689.

Abstract

RecF, RecO and RecR, three of the important proteins of the RecF pathway of recombination, are also needed for repair of DNA damage due to UV irradiation. recF mutants are not proficient in cleaving LexA repressor in vivo following DNA damage: therefore they show a delay of induction of the SOS response. In this communication, by measuring the in vivo levels of LexA repressor using anti-LexA antibodies, we show that recO and recR mutant strains are also not proficient in LexA cleavage reactions. In addition, we show that recO and recR mutations delay induction of beta-galactosidase activity expressed from a lexA-regulated promoter following exposure of cells to UV, thus further supporting the idea that recF, recO and recR gene products are needed for induction of the SOS response.

摘要

RecF、RecO和RecR是重组RecF途径的三种重要蛋白质,也是紫外线照射导致的DNA损伤修复所必需的。recF突变体在DNA损伤后体内不能有效地切割LexA阻遏物:因此它们表现出SOS反应诱导延迟。在本通讯中,通过使用抗LexA抗体测量LexA阻遏物的体内水平,我们表明recO和recR突变株在LexA切割反应中也不高效。此外,我们表明recO和recR突变会延迟细胞暴露于紫外线后从lexA调控启动子表达的β-半乳糖苷酶活性的诱导,从而进一步支持recF、recO和recR基因产物是SOS反应诱导所必需的这一观点。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验