A Ca2+-sensor switch for tolerance to elevated salt stress in Arabidopsis

Steinhorst, Leonie; He, Gefeng; Moore, Lena K.; Schültke, Stefanie; Schmitz-Thom, Ina; Cao, Yibo; Hashimoto, Kenji; Andrés, Zaida; Piepenburg, K.; Ragel, Paula; Behera, Smrutisanjita; Almutairi, Bader O.; Batistič, Oliver; Wyganowski, Thomas; Köster, Philipp; Edel, Kai H.; Zhang, Chunxia; Krebs, Melanie; Jiang, Caifu; Guo, Yan; Quintero, Francisco J.; Bock, R.; Kudla, Jörg

doi:10.1016/j.devcel.2022.08.001

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A Ca2+-sensor switch for tolerance to elevated salt stress in Arabidopsis

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Piepenburg, K.
Organelle Biology and Biotechnology, Department Bock, Max Planck Institute of Molecular Plant Physiology, Max Planck Society;

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Bock, R.
Organelle Biology and Biotechnology, Department Bock, Max Planck Institute of Molecular Plant Physiology, Max Planck Society;

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Steinhorst, L., He, G., Moore, L. K., Schültke, S., Schmitz-Thom, I., Cao, Y., et al. (2022). A Ca2+-sensor switch for tolerance to elevated salt stress in Arabidopsis. Developmental Cell, 57(17), 2081-2094. doi:10.1016/j.devcel.2022.08.001.

Cite as: https://hdl.handle.net/21.11116/0000-000A-E9C9-D

Abstract

Summary
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.