Mechanisms of calcium homeostasis orchestrate plant growth and immunity.

Calcium (Ca 2+ ) 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 Ca 2+ homeostasis by regulating numerous Ca 2+ transporters 3 . Here we report two signalling pathways in Arabidopsis thaliana that converge on the activation of vacuolar Ca 2+ /H + exchangers (CAXs) to scavenge excess cytosolic Ca 2+ in plants. One mechanism, activated in response to an elevated external Ca 2+ level, entails calcineurin B-like (CBL) Ca 2+ 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 Ca 2+ signals in immunity. These Ca 2+ -dependent (CBL-CIPK) and Ca 2+ -independent (FLS2-BAK1-BIK1/PBL1) mechanisms combine to balance plant growth and immunity by regulating cytosolic Ca 2+ homeostasis.