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Excessive Na+ in soils inhibits plant growth. 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. 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. 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. 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. 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. [Display omitted] • In Arabidopsis , Na+ specifically induces primary Ca2+ signals in a sodium-sensing niche • Ca2+-signal amplitudes and Ca2+ wave speed quantitatively reflect stress intensity • CBL8 particularly contributes to salt tolerance under high-salt-stress conditions • CBL8 functions as Ca2+-sensor switch for enhanced SOS pathway efficiency Salt stress is detrimental to plants. Steinhorst et al. reveal how plants measure salt stress intensity. The authors report that stress intensity quantitatively determines Ca2+-signal amplitude and delineates a signal-intensity-dependent Ca2+-sensor switch in Arabidopsis , allowing for efficient fine tuning of adaptive salt tolerance. [ABSTRACT FROM AUTHOR]

Organismal homeostasis of the essential ion K+ requires sensing of its availability, efficient uptake, and defined distribution. Understanding plant K+ nutrition is essential to advance sustainable agriculture, but the mechanisms underlying K+ sensing and the orchestration of downstream responses have remained largely elusive. Here, we report where plants sense K+ deprivation and how this translates into spatially defined ROS signals to govern specific downstream responses. We define the organ-scale K+ pattern of roots and identify a postmeristematic K+-sensing niche (KSN) where rapid K+ decline and Ca2+ signals coincide. Moreover, we outline a bifurcating low-K+-signaling axis of CIF peptide-activated SGN3-LKS4/SGN1 receptor complexes that convey low-K+-triggered phosphorylation of the NADPH oxidases RBOHC, RBOHD, and RBOHF. The resulting ROS signals simultaneously convey HAK5 K+ uptake-transporter induction and accelerated Casparian strip maturation. Collectively, these mechanisms synchronize developmental differentiation and transcriptome reprogramming for maintaining K+ homeostasis and optimizing nutrient foraging by roots. [Display omitted] • K+ deprivation triggers rapid K+ and Ca2+ signals in the root KSN • Ca2+ induces CIF peptides to activate SGN3-LKS4/SGN1 receptor complexes • LKS4 phosphorylates and activates RBOHC/D/F for ROS signal formation • ROS signals convey HAK5 K+ transporter induction and accelerated CS maturation Wang et al. investigate where and how plants sense and implement responses to insufficient supply of the essential nutrient potassium (K+). The authors identify a Ca2+-triggered CIF peptide-RLK-NOX signaling axis that synchronizes root developmental differentiation with transcriptome reprograming for maintaining plant K+ homeostasis. [ABSTRACT FROM AUTHOR]