Genetic evidence for histidine kinase HP165 being an acid sensor of Helicobacter pylori

Genetic evidence for histidine kinase HP165 being an acid sensor of Helicobacter pylori
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DOI:
10.1016/j.femsle.2004.03.023
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发表时间:
2004-05-01
影响因子:
2.1
通讯作者:
Beier, D
Beier, D
中科院分区:
生物学4区
文献类型:
--
作者:
Pflock, M;Dietz, P;Beier, D

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幽门螺杆菌是一种非常适应其独特生境的人类胃病原体。在胃中普遍存在的酸性条件下生存的关键是尿素酶。转录组分析表明,大量基因的转录响应于H。pylori转化为酸的基因,包括编码尿素酶亚基UreA和UreB的基因以及先前已经鉴定的Lis双组分系统HP 166-HP 165的靶基因的几个基因。在此,我们提供了组氨酸激酶HP 165感受到的刺激是pH的遗传证据,因为在酸性pH下,控制属于HP 166-HP 165调节子的ORF hp 119和hp 1432表达的启动子的转录增加严格依赖于组氨酸激酶HP 165的存在。此外,我们表明,从ureA基因启动子的基础转录是由HP 166-HP 165双组分系统调节,以响应酸性pH。另一方面,酸诱导的转录增加的启动子指导孤儿反应调节因子HP 1021的表达不是由HP 166-HP 165双组分系统控制,也不是由HP 1021本身介导的。(C)2004年,欧洲微生物学会联合会。Elsevier B. V.出版,保留所有权利。
Helicobacter pylori is a human gastric pathogen which is extremely well adapted to its unique habitat. Crucial for the survival under the acidic conditions prevailing in the stomach is the enzyme Urease. Transcriptome analysis has shown that transcription of a large number of genes responds to the exposure of H. pylori to acid including the genes encoding the urease Subunits UreA and UreB as well Lis several genes which have been previously identified Lis target genes of the two-component system HP166-HP165. Here, we 44 provide genetic evidence that a stimulus perceived by the histidine kinase HP165 is pH since increased transcription at acidic pH from the promoters controlling the expression of the ORFs hp119 and hp1432 which belong to the HP166-HP165 regulon is strictly dependent on the presence of histidine kinase HP165. Furthermore, we show that the basal transcription from the promoter of the ureA gene is modulated by the HP166-HP165 two-component system in response to acidic pH. On the other hand, the acid-induced increase in transcription of the promoter directing the expression of the orphan response regulator HP1021 is not controlled by the HP166-HP165 two-component system, nor is it mediated by HP1021 itself. (C) 2004 Federation of European Microbiological Societies. Published by Elsevier B.V. All rights reserved.