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组氨酸激酶与其同源应答调节因子之间的变构调节决定细胞命运。

Allosteric regulation of histidine kinases by their cognate response regulator determines cell fate.

作者信息

Paul Ralf, Jaeger Tina, Abel Sören, Wiederkehr Irene, Folcher Marc, Biondi Emanuele G, Laub Michael T, Jenal Urs

机构信息

Biozentrum, University of Basel, Klingelbergstrasse 70, 4056 Basel, Switzerland.

出版信息

Cell. 2008 May 2;133(3):452-61. doi: 10.1016/j.cell.2008.02.045.

DOI:10.1016/j.cell.2008.02.045
PMID:18455986
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2804905/
Abstract

The two-component phosphorylation network is of critical importance for bacterial growth and physiology. Here, we address plasticity and interconnection of distinct signal transduction pathways within this network. In Caulobacter crescentus antagonistic activities of the PleC phosphatase and DivJ kinase localized at opposite cell poles control the phosphorylation state and subcellular localization of the cell fate determinator protein DivK. We show that DivK functions as an allosteric regulator that switches PleC from a phosphatase into an autokinase state and thereby mediates a cyclic di-GMP-dependent morphogenetic program. Through allosteric activation of the DivJ autokinase, DivK also stimulates its own phosphorylation and polar localization. These data suggest that DivK is the central effector of an integrated circuit that operates via spatially organized feedback loops to control asymmetry and cell fate determination in C. crescentus. Thus, single domain response regulators can facilitate crosstalk, feedback control, and long-range communication among members of the two-component network.

摘要

双组分磷酸化网络对于细菌的生长和生理机能至关重要。在此,我们探讨该网络内不同信号转导途径的可塑性和相互联系。在新月柄杆菌中,位于相对细胞极的PleC磷酸酶和DivJ激酶的拮抗活性控制着细胞命运决定蛋白DivK的磷酸化状态和亚细胞定位。我们发现DivK作为一种变构调节因子,可将PleC从磷酸酶状态转变为自身激酶状态,从而介导一个依赖环二鸟苷酸的形态发生程序。通过变构激活DivJ自身激酶,DivK还能刺激自身的磷酸化和极性定位。这些数据表明,DivK是一个集成电路的核心效应器,该集成电路通过空间组织的反馈回路来控制新月柄杆菌中的不对称性和细胞命运决定。因此,单结构域应答调节因子可促进双组分网络成员之间的串扰、反馈控制和远程通信。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99b0/2804905/8a4f97fab322/nihms165295f7.jpg
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本文引用的文献

1
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Genes Dev. 2008 Jan 15;22(2):212-25. doi: 10.1101/gad.1601808.
2
Structure of BeF3- -modified response regulator PleD: implications for diguanylate cyclase activation, catalysis, and feedback inhibition.BeF₃⁻修饰的应答调节蛋白PleD的结构:对二鸟苷酸环化酶激活、催化及反馈抑制的影响
Structure. 2007 Aug;15(8):915-27. doi: 10.1016/j.str.2007.06.016.
3
Activation of the diguanylate cyclase PleD by phosphorylation-mediated dimerization.通过磷酸化介导的二聚化激活双鸟苷酸环化酶PleD。
J Biol Chem. 2007 Oct 5;282(40):29170-7. doi: 10.1074/jbc.M704702200. Epub 2007 Jul 19.
4
Regulation of the bacterial cell cycle by an integrated genetic circuit.通过整合基因回路对细菌细胞周期进行调控。
Nature. 2006 Dec 14;444(7121):899-904. doi: 10.1038/nature05321. Epub 2006 Nov 29.
5
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J Bacteriol. 2006 Jul;188(14):5315-8. doi: 10.1128/JB.01725-05.
6
Two-component signal transduction pathways regulating growth and cell cycle progression in a bacterium: a system-level analysis.调节细菌生长和细胞周期进程的双组分信号转导途径:系统水平分析
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7
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9
Cytokinesis monitoring during development; rapid pole-to-pole shuttling of a signaling protein by localized kinase and phosphatase in Caulobacter.发育过程中的胞质分裂监测;在柄杆菌中,一种信号蛋白通过局部激酶和磷酸酶进行快速的极到极穿梭。
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10
Dare to be different: asymmetric cell division in Drosophila, C. elegans and vertebrates.勇于与众不同:果蝇、秀丽隐杆线虫和脊椎动物中的不对称细胞分裂
Curr Biol. 2004 Aug 24;14(16):R674-85. doi: 10.1016/j.cub.2004.08.017.