通过LexA、RecA和SulA蛋白动力学分析紫外线照射的大肠杆菌中SOS反应的诱导情况。
Induction of the SOS Response in Ultraviolet-Irradiated Escherichia coli Analyzed by Dynamics of LexA, RecA and SulA Proteins.
作者信息
Aksenov S V
机构信息
Division of Radiation and Radiobiological Research, Joint Institute for Nuclear Research, 141980 Dubna, Moscow region, Russia; Tel.: +
出版信息
J Biol Phys. 1999 Jun;25(2-3):263-77. doi: 10.1023/A:1005163310168.
Abstract
The SOS response in Escherichia coli is induced after DNA-damaging treatments including ultraviolet light. Regulation of the SOS response is accomplished through specific interaction of the two SOS regulator proteins, LexA and RecA. In ultraviolet light-treated cells, nucleotide excision repair is the major system that removes the induced lesions from the DNA. Here, induction of the SOS response in Escherichia coli with normal and impaired excision repair function is studied by simulation of intracellular levels of regulatory LexA and RecA proteins, and SulA protein. SulA protein is responsible for SOS-inducible cell division inhibition. Results of the simulations show that nucleotide excision repair influences time-courses of LexA, RecA and SulA induction by modulating the dynamics of RecA protein distribution between its normal and SOS-activated forms.
摘要
大肠杆菌中的SOS应答在包括紫外线在内的DNA损伤处理后被诱导。SOS应答的调节是通过两种SOS调节蛋白LexA和RecA的特异性相互作用来完成的。在紫外线处理的细胞中，核苷酸切除修复是从DNA中去除诱导损伤的主要系统。在此，通过模拟调节性LexA、RecA蛋白和SulA蛋白的细胞内水平，研究了具有正常和受损切除修复功能的大肠杆菌中SOS应答的诱导情况。SulA蛋白负责SOS诱导的细胞分裂抑制。模拟结果表明，核苷酸切除修复通过调节RecA蛋白在其正常形式和SOS激活形式之间的分布动态，影响LexA、RecA和SulA诱导的时间进程。
相似文献
1
Induction of the SOS Response in Ultraviolet-Irradiated Escherichia coli Analyzed by Dynamics of LexA, RecA and SulA Proteins.通过LexA、RecA和SulA蛋白动力学分析紫外线照射的大肠杆菌中SOS反应的诱导情况。
J Biol Phys. 1999 Jun;25(2-3):263-77. doi: 10.1023/A:1005163310168.
2
Regulation of the SOS response in Bacillus subtilis: evidence for a LexA repressor homolog.枯草芽孢杆菌中SOS反应的调控：LexA阻遏物同源物的证据。
J Bacteriol. 1991 Oct;173(20):6489-98. doi: 10.1128/jb.173.20.6489-6498.1991.
3
SOS induction of the gene sulA is partly inhibited in Escherichia coli K12 cells overproducing the RecA protein.
Mutat Res. 1986 Sep;175(1):17-21. doi: 10.1016/0165-7992(86)90139-9.
4
Novel mechanism for UV sensitivity and apparent UV nonmutability of recA432 mutants: persistent LexA cleavage following SOS induction.recA432突变体对紫外线敏感及明显的紫外线不可突变性的新机制：SOS诱导后LexA持续切割
J Bacteriol. 1993 Nov;175(22):7373-82. doi: 10.1128/jb.175.22.7373-7382.1993.
5
Mathematical model of the SOS response regulation of an excision repair deficient mutant of Escherichia coli after ultraviolet light irradiation.紫外线照射后大肠杆菌切除修复缺陷突变体SOS反应调控的数学模型
J Theor Biol. 1997 May 21;186(2):251-60. doi: 10.1006/jtbi.1996.0353.
6
Efficient repair of hydrogen peroxide-induced DNA damage by Escherichia coli requires SOS induction of RecA and RuvA proteins.大肠杆菌对过氧化氢诱导的DNA损伤进行有效修复需要SOS诱导RecA和RuvA蛋白。
Mutat Res. 2000 Apr 28;459(3):187-94. doi: 10.1016/s0921-8777(99)00073-7.
7
Constitutive expression of the SOS response in recA718 mutants of Escherichia coli requires amplification of RecA718 protein.在大肠杆菌recA718突变体中，SOS反应的组成型表达需要RecA718蛋白的扩增。
J Bacteriol. 1987 Feb;169(2):728-34. doi: 10.1128/jb.169.2.728-734.1987.
8
Dual role for Escherichia coli RecA protein in SOS mutagenesis.大肠杆菌RecA蛋白在SOS诱变中的双重作用。
Proc Natl Acad Sci U S A. 1985 May;82(10):3325-9. doi: 10.1073/pnas.82.10.3325.
9
Interaction of Escherichia coli RecA protein with LexA repressor. II. Inhibition of DNA strand exchange by the uncleavable LexA S119A repressor argues that recombination and SOS induction are competitive processes.大肠杆菌RecA蛋白与LexA阻遏物的相互作用。II. 不可裂解的LexA S119A阻遏物对DNA链交换的抑制表明重组和SOS诱导是竞争性过程。
J Biol Chem. 1996 Sep 27;271(39):23874-83.
10
Functional recA, lexA, umuD, umuC, polA, and polB genes are not required for the Escherichia coli UVM response.大肠杆菌UVM反应不需要功能性recA、lexA、umuD、umuC、polA和polB基因。
J Bacteriol. 1995 Nov;177(21):6041-8. doi: 10.1128/jb.177.21.6041-6048.1995.
引用本文的文献
1
Dysregulated DnaB unwinding induces replisome decoupling and daughter strand gaps that are countered by RecA polymerization.DNA 解旋酶调控失调导致复制体解偶联和子链缺口，这些问题可以通过 RecA 聚合来解决。
Nucleic Acids Res. 2024 Jul 8;52(12):6977-6993. doi: 10.1093/nar/gkae435.
2
Antimicrobial growth promoters approved in food-producing animals in South Africa induce shiga toxin-converting bacteriophages from Escherichia coli O157:H7.在南非，用于食用动物的抗菌生长促进剂会诱导大肠杆菌O157:H7产生志贺毒素转换噬菌体。
Gut Pathog. 2023 Dec 6;15(1):64. doi: 10.1186/s13099-023-00590-9.
3
Adaptive Radioresistance of Enterohemorrhagic Escherichia coli O157:H7 Results in Genomic Loss of Shiga Toxin-Encoding Prophages.肠出血性大肠杆菌 O157:H7 的适应性放射抗性导致编码志贺毒素的噬菌体基因组丢失。
Appl Environ Microbiol. 2023 Apr 26;89(4):e0130622. doi: 10.1128/aem.01306-22. Epub 2023 Apr 4.
4
Resistance of Bacteria toward 475 nm Blue Light Exposure and the Possible Role of the SOS Response.细菌对475纳米蓝光照射的抗性及SOS反应的可能作用
Life (Basel). 2022 Sep 26;12(10):1499. doi: 10.3390/life12101499.
5
Naturalized in Wastewater and the Co-evolution of Bacterial Resistance to Water Treatment and Antibiotics.在废水中归化以及细菌对水处理和抗生素耐药性的共同进化
Front Microbiol. 2022 May 30;13:810312. doi: 10.3389/fmicb.2022.810312. eCollection 2022.
6
Adaptive Resistance Mutations at Suprainhibitory Concentrations Independent of SOS Mutagenesis.超抑制浓度下独立于 SOS 诱变的适应性耐药突变。
Mol Biol Evol. 2021 Sep 27;38(10):4095-4115. doi: 10.1093/molbev/msab196.
7
Novel Genes Involved in Resistance to Both Ultraviolet Radiation and Perchlorate From the Metagenomes of Hypersaline Environments.来自高盐环境宏基因组中与抗紫外线辐射和高氯酸盐相关的新基因。
Front Microbiol. 2020 Mar 26;11:453. doi: 10.3389/fmicb.2020.00453. eCollection 2020.
8
Threshold effect of growth rate on population variability of cell lengths.生长速率对细胞长度群体变异性的阈值效应。
R Soc Open Sci. 2017 Feb 22;4(2):160417. doi: 10.1098/rsos.160417. eCollection 2017 Feb.
9
Cooperativity of Negative Autoregulation Confers Increased Mutational Robustness.负向自动调节的协同作用赋予更高的突变稳健性。
Phys Rev Lett. 2016 Jun 24;116(25):258104. doi: 10.1103/PhysRevLett.116.258104. Epub 2016 Jun 22.
10
Simulating the temporal modulation of inducible DNA damage response in Escherichia coli.模拟大肠杆菌中诱导性DNA损伤反应的时间调控
Biophys J. 2007 Jul 1;93(1):62-73. doi: 10.1529/biophysj.106.090712. Epub 2007 Apr 13.
本文引用的文献
1
Dynamics of the inducing signal for the SOS regulatory system in Escherichia coli after ultraviolet irradiation.
Math Biosci. 1999 Mar 15;157(1-2):269-86. doi: 10.1016/s0025-5564(98)10086-x.
2
Mathematical model of the SOS response regulation of an excision repair deficient mutant of Escherichia coli after ultraviolet light irradiation.紫外线照射后大肠杆菌切除修复缺陷突变体SOS反应调控的数学模型
J Theor Biol. 1997 May 21;186(2):251-60. doi: 10.1006/jtbi.1996.0353.
3
recO and recR mutations delay induction of the SOS response in Escherichia coli.recO和recR突变会延迟大肠杆菌中SOS反应的诱导。
Mol Gen Genet. 1995 Jan 20;246(2):254-8. doi: 10.1007/BF00294689.
4
Mechanism of action of the lexA gene product.lexA基因产物的作用机制。
Proc Natl Acad Sci U S A. 1981 Jul;78(7):4204-8. doi: 10.1073/pnas.78.7.4204.
5
An inducible DNA replication-cell division coupling mechanism in E. coli.大肠杆菌中的一种可诱导的DNA复制-细胞分裂偶联机制。
Nature. 1981 Apr 30;290(5809):797-9. doi: 10.1038/290797a0.
6
How Escherichia coli sets different basal levels in SOS operons.大肠杆菌如何在SOS操纵子中设定不同的基础水平。
Biochimie. 1982 Aug-Sep;64(8-9):709-12. doi: 10.1016/s0300-9084(82)80115-6.
7
Regulation and autoregulation by lexA protein.LexA蛋白的调控与自动调控。
Biochimie. 1982 Aug-Sep;64(8-9):565-9. doi: 10.1016/s0300-9084(82)80088-6.
8
E. coli recA protein-directed cleavage of phage lambda repressor requires polynucleotide.大肠杆菌RecA蛋白介导的噬菌体λ阻遏物切割需要多核苷酸。
Nature. 1980 Jan 3;283(5742):26-30. doi: 10.1038/283026a0.
9
Mutagenesis and inducible responses to deoxyribonucleic acid damage in Escherichia coli.大肠杆菌中的诱变作用及对脱氧核糖核酸损伤的诱导反应
Microbiol Rev. 1984 Mar;48(1):60-93. doi: 10.1128/mr.48.1.60-93.1984.
10
Induction by UV light of the SOS function sfiA in Escherichia coli strains deficient or proficient in excision repair.紫外线诱导大肠杆菌中切除修复缺陷或正常的菌株产生SOS功能sfiA。
J Bacteriol. 1984 Jan;157(1):35-8. doi: 10.1128/jb.157.1.35-38.1984.
Zotero 插件