ABA-activated low-nanomolar Ca(2+)-CPK signalling controls root cap cycle plasticity and stress adaptation.

Abscisic acid (ABA) regulates plant stress adaptation, growth and reproduction. Despite extensive ABA-Ca(2+) signalling links, imaging ABA-induced increases in Ca(2+) concentration has been challenging, except in guard cells. Here we visualize ABA-triggered [Ca(2+)] dynamics in diverse organs and cell types of Arabidopsis thaliana using a genetically encoded Ca(2+) ratiometric sensor with a low-nanomolar Ca(2+)-binding affinity and a large dynamic range. The subcellular-targeted Ca(2+) ratiometric sensor reveals time-resolved and unique spatiotemporal Ca(2+) signatures from the initial plasma-membrane nanodomain, to cytosol, to nuclear oscillation. Via receptors and sucrose-non-fermenting1-related protein kinases (SnRK2.2/2.3/2.6), ABA activates low-nanomolar Ca(2+) transient and Ca(2+)-sensor protein kinase (CPK10/30/32) signalling in the root cap cycle from stem cells to cell detachment. Surprisingly, unlike the prevailing NaCl-stimulated micromolar Ca(2+) spike, salt stress induces a low-nanomolar Ca(2+) transient through ABA signalling, repressing key transcription factors that dictate cell fate and enzymes that are crucial to root cap maturation and slough. Our findings uncover ABA-Ca(2+)-CPK signalling that modulates root cap cycle plasticity in adaptation to adverse environments.