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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Receptor density balances signal stimulation and attenuation in membrane-assembled complexes of bacterial chemotaxis signaling proteins
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Receptor density balances signal stimulation and attenuation in membrane-assembled complexes of bacterial chemotaxis signaling proteins

机译：受体密度平衡细菌趋化信号蛋白膜组装复合物中的信号刺激和衰减。

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摘要

All cells possess transmembrane signaling systems that function in the environment of the lipid bilayer. In the Escherichia coli chemotaxis pathway, the binding of attractants to a two-dimensional array of receptors and signaling proteins simultaneously inhibits an associated kinase and stimulates receptor methylation-a slower process that restores kinase activity. These two opposing effects lead to robust adaptation toward stimuli through a physical mechanism that is not understood. Here, we provide evidence of a counterbalancing influence exerted by receptor density on kinase stimulation and receptor methylation. Receptor signaling complexes were reconstituted over a range of defined surface concentrations by using a template-directed assembly method, and the kinase and receptor methylation activities were measured. Kinase activity and methylation rates were both found to vary significantly with surface concentration-yet in opposite ways: samples prepared at high surface densities stimulated kinase activity more effectively than low-density samples, whereas lower surface densities produced greater methylation rates than higher densities. FRET experiments demonstrated that the cooperative change in kinase activity coincided with a change in the arrangement of the membrane-associated receptor domains. The counterbalancing influence of density on receptor methylation and kinase stimulation leads naturally to a model for signal regulation that is compatible with the known logic of the E. coli pathway. Density-dependent mechanisms are likely to be general and may operate when two or more membrane-related processes are influenced differently by the two-dimensional concentration of pathway elements.
机译：所有细胞都具有在脂双层环境中起作用的跨膜信号传导系统。在大肠杆菌的趋化途径中，引诱剂与受体和信号蛋白的二维阵列的结合同时抑制相关的激酶并刺激受体甲基化-恢复激酶活性的较慢过程。这两种相反的作用通过未知的物理机制导致对刺激的鲁棒适应。在这里，我们提供了受体密度对激酶刺激和受体甲基化产生的平衡影响的证据。通过使用模板指导的组装方法，在一定范围的表面浓度范围内重构受体信号复合物，并测量激酶和受体的甲基化活性。发现激酶活性和甲基化速率均随表面浓度而显着变化，但是以相反的方式：以高表面密度制备的样品比低密度样品更有效地刺激了激酶活性，而较低的表面密度比较高的密度产生更高的甲基化速率。 FRET实验表明，激酶活性的协同变化与膜相关受体结构域的排列变化同时发生。密度对受体甲基化和激酶刺激的平衡影响自然会导致与大肠杆菌途径的已知逻辑兼容的信号调节模型。依赖于密度的机制很可能是通用的，并且当两个或多个与膜相关的过程受到路径元素二维浓度的不同影响时，可能会起作用。

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