Mechanisms of calcium homeostasis orchestrate plant growth and immunity.

Abstract

Calcium (Ca²⁺) is an essential nutrient for plants and a cellular signal, but excessive levels can be toxic and inhibit growth^1,2. To thrive in dynamic environments, plants must monitor and maintain cytosolic Ca²⁺ homeostasis by regulating numerous Ca²⁺ transporters³. Here we report two signalling pathways in Arabidopsis thaliana that converge on the activation of vacuolar Ca²⁺/H⁺ exchangers (CAXs) to scavenge excess cytosolic Ca²⁺ in plants. One mechanism, activated in response to an elevated external Ca²⁺ level, entails calcineurin B-like (CBL) Ca²⁺ sensors and CBL-interacting protein kinases (CIPKs), which activate CAXs by phosphorylating a serine (S) cluster in the auto-inhibitory domain. The second pathway, triggered by molecular patterns associated with microorganisms, engages the immune receptor complex FLS2-BAK1 and the associated cytoplasmic kinases BIK1 and PBL1, which phosphorylate the same S-cluster in CAXs to modulate Ca²⁺ signals in immunity. These Ca²⁺-dependent (CBL-CIPK) and Ca²⁺-independent (FLS2-BAK1-BIK1/PBL1) mechanisms combine to balance plant growth and immunity by regulating cytosolic Ca²⁺ homeostasis.