The EAL domain protein YciR acts as a trigger enzyme in a c-di-GMP signalling cascade in E. coli biofilm control.

The EAL domain protein YciR acts as a trigger enzyme in a c-di-GMP signalling cascade in E. coli biofilm control.
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EAL结构域蛋白YCIR充当大肠杆菌生物膜对照中C-DI-GMP信号级联反应中的触发酶。

DOI:
10.1038/emboj.2013.120
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发表时间:
2013-07-17
期刊:
影响因子:
11.4
通讯作者:
Hengge, Regine
Hengge, Regine
中科院分区:
生物学1区
文献类型:
--
作者:
Lindenberg, Sandra;Klauck, Gisela;Pesavento, Christina;Klauck, Eberhard;Hengge, Regine

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由二鸟苷酸环化酶(DGC)产生并被特异性磷酸二酯酶(PDE)降解的C-di-GMP是细菌生物膜形成过程中普遍存在的第二信使。在大肠杆菌中,几种DGC(YegE,YdaM)和PDE(YhjH,YciR)以及MerR样转录因子MlrA调节csgD的转录,csgD编码生物膜基质的淀粉样卷曲纤维产生所必需的生物膜调节剂。在这里,我们表明,该系统作为一个信号级联,其中c-di-GMP控制的DGC/PDE对YegE/YhjH(模块I)调节活性的YdaM/YciR对(模块II)。通过多重直接相互作用,两个模块II蛋白与MlrA形成信号传导复合物。YciR作为模块I和II之间的连接器,并作为触发酶发挥作用:当其结合并降解模块I产生的c-di-GMP时,其对DGC YdaM的直接抑制被解除。因此,YdaM随后产生c-di-GMP,并通过直接和特异性的相互作用激活MlrA以刺激csgD转录。触发酶可能代表局部c-di-GMP信号传导的一般原理。
C-di-GMP—which is produced by diguanylate cyclases (DGC) and degraded by specific phosphodiesterases (PDEs)—is a ubiquitous second messenger in bacterial biofilm formation. In Escherichia coli, several DGCs (YegE, YdaM) and PDEs (YhjH, YciR) and the MerR-like transcription factor MlrA regulate the transcription of csgD, which encodes a biofilm regulator essential for producing amyloid curli fibres of the biofilm matrix. Here, we demonstrate that this system operates as a signalling cascade, in which c-di-GMP controlled by the DGC/PDE pair YegE/YhjH (module I) regulates the activity of the YdaM/YciR pair (module II). Via multiple direct interactions, the two module II proteins form a signalling complex with MlrA. YciR acts as a connector between modules I and II and functions as a trigger enzyme: its direct inhibition of the DGC YdaM is relieved when it binds and degrades c-di-GMP generated by module I. As a consequence, YdaM then generates c-di-GMP and—by direct and specific interaction—activates MlrA to stimulate csgD transcription. Trigger enzymes may represent a general principle in local c-di-GMP signalling.
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发表时间: 2007-09
期刊: PLOS GENETICS
影响因子: 4.5
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影响因子: 11.1
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期刊: BIOINFORMATICS
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