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负责差异调控荚膜红细菌反应中心和光捕获I基因表达的光响应反式激活因子的特性分析

Characterization of a light-responding trans-activator responsible for differentially controlling reaction center and light-harvesting-I gene expression in Rhodobacter capsulatus.

作者信息

Buggy J J, Sganga M W, Bauer C E

机构信息

Department of Biology, Indiana University, Bloomington 47405.

出版信息

J Bacteriol. 1994 Nov;176(22):6936-43. doi: 10.1128/jb.176.22.6936-6943.1994.

DOI:10.1128/jb.176.22.6936-6943.1994
PMID:7961455
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC197064/
Abstract

The purple nonsulfur photosynthetic bacterium Rhodobacter capsulatus regulates synthesis of its photosystem in response to two environmental stimuli, oxygen tension and light intensity. Here we describe the identification and characterization of the trans-acting regulatory gene hvrA, which we show is involved in differentially controlling reaction center and light-harvesting gene expression in response to alterations in light intensity. An hvrA mutant strain is shown to lack the capability to trans-activate light-harvesting-I and reaction center gene expression but retain normal light-harvesting-II and photopigment regulation, in response to a reduction in light intensity. As a consequence of altered expression, hvrA mutant strains exhibit reduced photosynthetic growth capabilities under dim-light conditions. The results of this study and additional studies indicate that regulated synthesis of the photosystem involves complex sets of overlapping regulatory circuits that differentially control photosystem gene expression in response to environmental stimuli such as oxygen tension and light intensity.

摘要

紫色非硫光合细菌荚膜红细菌(Rhodobacter capsulatus)会根据氧气张力和光照强度这两种环境刺激来调节其光合系统的合成。在此,我们描述了反式作用调节基因hvrA的鉴定和特性,我们发现它参与了根据光照强度的变化来差异控制反应中心和捕光基因的表达。研究表明,hvrA突变菌株在光照强度降低时,缺乏反式激活捕光-I和反应中心基因表达的能力,但保留了正常的捕光-II和光合色素调节能力。由于表达改变,hvrA突变菌株在弱光条件下表现出光合生长能力下降。本研究及其他研究结果表明,光合系统的调节合成涉及复杂的重叠调节回路,这些回路根据氧气张力和光照强度等环境刺激来差异控制光合系统基因的表达。

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Null mutation of HvrA compensates for loss of an essential relA/spoT-like gene in Rhodobacter capsulatus.HvrA的无效突变可补偿荚膜红细菌中一个必需的relA/spoT样基因的缺失。
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