色氨酸操纵子调控机制详析  

A Detailed Analysis of the Regulatory Mechanism of the Tryptophan Operon

作　　者：冯慧 李红民[1,2] FENG Hui;LI Hong-Min(Department of Biological Sciences,School of Life Sciences,Northwest University,Xi’an 710069,China;Molecular Biology Course Group,Department of Biotechnology,School of Life Sciences,Northwest University,Xi’an 710069,China)

机构地区：[1]西北大学生命科学学院生物科学系,西安710069 [2]西北大学生命科学学院生物技术系分子生物学课程组,西安710069

出　　处：《中国生物化学与分子生物学报》2020年第1期6-13,共8页Chinese Journal of Biochemistry and Molecular Biology

基　　金：西北大学2018年度教学研究与成果重点培育项目(No.JX18053);陕西省高等教育学会2017年度高等教育科学研究项目(No.XGH17058)资助~~

摘　　要：色氨酸操纵子是最早被研究的细菌合成代谢调控、基因表达调控的模型之一。其中阻遏蛋白对转录起始的抑制作用、色氨酸作为辅阻遏物的作用以及通过定点突变揭示的弱化作用的分子机制已基本被阐明。此外,色氨酸操纵子RNA结合弱化蛋白、NusA、Nus G、Trp Y等调节蛋白对细菌色氨酸操纵子弱化作用的调节机制也在近年来得到进一步揭示。特别是在枯草芽孢杆菌中,色氨酸操纵子主要依赖于转录衰减机制调控,包括由色氨酸激活的色氨酸操纵子RNA结合弱化蛋白与新生转录产物结合形成内部终止子,导致5’非翻译区(5’UTR)转录终止。Nus A、Nus G通过刺激RNA聚合酶在5’UTR的U107和U144位点暂停,释放出RNA聚合酶,最终造成转录终止。不同的是,在U144位点NusA参与的转录弱化机制依赖其发夹结构,且NusA与RNA聚合酶作用促进了RNA结合弱化蛋白与新生转录产物的结合,使转录终止。而NusG是通过与非模板DNA链中的一段富含T碱基序列和RNA聚合酶同时互作,阻止了RNA聚合酶向下游移动,从而引起RNA聚合酶高效停滞。但在细菌操纵子中,绝大多数调节因子参与的弱化机制最终依赖于ρ因子,从而导致多达一半的转录终止事件发生。近年来,随着学科的发展,越来越多关于色氨酸操纵子调节机制新概念被挖掘报道,这也使人类对色氨酸操纵子的表达调控机制的认知愈加详尽。The tryptophan( trp) operon is one of the earliest study models applied to the regulation of bacterial bio-synthetic and gene expression. And the molecular mechanisms,including the inhibitory action of repressor on transcription initiation,the role of trp as a corepressor and the attenuation revealed by site-directed mutation,have been largely elucidated. Moreover,it has been demonstrated that the regulatory proteins,including the trp RNA-binding attenuation protein( TRAP),NusA,Nus G,TrpY,have attenuating effects on the trp operon,and the attenuation mechanisms have been uncovered recently.Notably,the trp operon in Bacillus subtilis is mainly regulated by the transcription attenuation mechanism.TRAP firstly binds to the nascent transcripts to form the intrinsic terminator and causes termination in the5’ untranslated region( 5’ UTR). Afterwards,NusA and Nus G stimulate the RNA polymerase to pause and release at U107 and U144 sites in 5’ UTR,which eventually results in transcription termination.However, there are some differences in NusA-and Nus G-stimulated RNA polymerase pausing mechanisms. The transcription attenuation mechanism regulated by NusA at U144 depends on the hairpin structure,and the interaction between NusA and the RNA polymerase promotes the binding of TRAP to the nascent transcripts and the transcription termination. NusG,on the other hand,touches a T-rich sequence in the non-template DNA( ntDNA) strand and RNA polymerase at the same time,which prevents forward movement of the RNA polymerase and causes dramatic RNA polymerase pausing.However,in the bacterial trp operon,up to half of the transcription termination events rely on the ρfactor. Here we summarize new concepts about the regulation mechanism of the trp operon with the development of related disciplines,and provide more in-depth details about the regulation mechanism of the tryptophan operon transcription.

关 键 词：色氨酸操纵子 弱化作用 色氨酸操纵子RNA结合弱化蛋白 NUSA NUSG 

分 类 号：Q936[生物学—微生物学]