背景回顾：Excessive Na⁺ in soils inhibits plant growth. 

主要发现：Here, we report that Na⁺ stress triggers primary calcium signals specifically in a cell group within the root differentiation zone, thus forming a “sodium-sensing niche” in Arabidopsis. 

结果1-钙离子信号的剂量效应：The amplitude of this primary calcium signal and the speed of the resulting Ca²⁺ wave dose-dependently increase with rising Na⁺ concentrations, thus providing quantitative information about the stress intensity encountered. 

结果2-不同盐胁迫下的钙离子感知：We also delineate a Ca²⁺-sensing mechanism that measures the stress intensity in order to mount appropriate salt detoxification responses. This is mediated by a Ca²⁺-sensor-switch mechanism, in which the sensors SOS3/CBL4 and CBL8 are activated by distinct Ca²⁺-signal amplitudes. 

结果3-基础模块和增强模块：Although the SOS3/CBL4-SOS2/CIPK24-SOS1 axis confers basal salt tolerance, the CBL8-SOS2/CIPK24-SOS1 module becomes additionally activated only in response to severe salt stress. 

结论：Thus, Ca²⁺-mediated translation of Na⁺ stress intensity into SOS1 Na⁺/H⁺ antiporter activity facilitates fine tuning of the sodium extrusion capacity for optimized salt-stress tolerance.

 摘 要 

土壤中过多的钠离子会抑制植物的生长。本文中，作者发现钠离子胁迫会诱导拟南芥根分生区中一类细胞的特异性初级钙离子信号，从而形成一个“钠感应微环境”。初级钙离子信号的幅度和钙离子波的扩散速度随着钠离子浓度的增加而增强，从而对所遭遇的胁迫强度进行定量感知。作者还揭示了一个测量胁迫强度的钙离子感知机制，从而启动适当的盐解毒响应。该过程是由一个钙离子感知开关机制所介导的，其中感应器SOS3/CBL4和CBL8受到不同的钙离子信号幅度所激活。尽管SOS3/CBL4-SOS2/CIPK24-SOS1赋予基础的盐胁迫耐受性，CBL8-SOS2/CIPK24-SOS1模块仅在响应严重盐胁迫时被额外激活。因此，钙离子介导的钠离子胁迫强度转化成SOS1钠离子/氢离子逆转运体活性，促进钠排出能力的精细调控，从而最优化盐胁迫耐受性。

 Jörg Kudla