Fig. 3. Current model of osmotic stress kinases network and signalling pathways.

Osmotic stress evokes rapid increase of Ca²⁺, which is perceived by OSCA1 osmosensor proteins localized at plasma membrane. Question marks in violet objects depict possible downstream components activated by OSCA1 in response to osmotic stress. Raf-like kinases are activated in response to osmotic stress likely via other uncharacterized osmosensor proteins depicted as question mark in black box. B4 Raf-like MAPKKKs phosphorylate and activate subclass I SnRK2s, which are not responsive to ABA, and in turn SnRK2s phosphorylate mRNA binding proteins, such as VCS, which forms a protein complex with the decapping proteins DCP1 and DCP2 and are involved in post-transcriptional regulation of mRNA in p-bodies. B2/B3 Raf-like MAPKKKs phosphorylate and activate subclass III SnRK2s, which are ABA-responsive. In the presence of ABA, PYR/PYL/RCAR receptors form protein complexes with PP2C, resulting in the release of subclass III SnRK2s from inhibition by PP2Cs. Subclass III SnRK2s, phosphorylate SLAC1, KAT1 and RBOHF membrane proteins, which are essential for stomatal aperture regulation. Subclass III SnRK2s phosphorylate AREB/ABF transcription factors, which in turn activate the expression of stress-responsive genes. DREB2A transcription factor is activated through an ABA-independent signalling pathway. Question mark pink box depicts plausible upstream regulators of DREB2A still unknown. Straight arrows indicate direct interaction and phosphorylation, dashed arrows (black) indicate putative interactions not fully experimentally validated in vivo, and dashed arrows (grey) depict ion flux through membrane channel proteins. Double arrowhead dashed arrow indicates association–dissociation of PP2C with SnRK2s in the absence–presence of ABA.