Upstream kinases of plant SnRKs are involved in salt stress tolerance

Abstract

SummarySucrose non‐fermenting 1‐related protein kinases (SnRKs) are important for plant growth and stress responses. This family has three clades: SnRK1, SnRK2 and SnRK3. Although plant SnRKs are thought to be activated by upstream kinases, the overall mechanism remains obscure. Geminivirus Rep‐Interacting Kinase (GRIK)1 and GRIK2 phosphorylate SnRK1s, which are involved in sugar/energy sensing, and the grik1‐1 grik2‐1 double mutant shows growth retardation under regular growth conditions. In this study, we established another Arabidopsis mutant line harbouring a different allele of gene GRIK1 (grik1‐2 grik2‐1) that grows similarly to the wild‐type, enabling us to evaluate the function of GRIKs under stress conditions. In the grik1‐2 grik2‐1 double mutant, phosphorylation of SnRK1.1 was reduced, but not eliminated, suggesting that the grik1‐2 mutation is a weak allele. In addition to high sensitivity to glucose, the grik1‐2 grik2‐1 mutant was sensitive to high salt, indicating that GRIKs are also involved in salinity signalling pathways. Salt Overly Sensitive (SOS)2, a member of the SnRK3 subfamily, is a critical mediator of the response to salinity. GRIK1 phosphorylated SOS2 in vitro, resulting in elevated kinase activity of SOS2. The salt tolerance of sos2 was restored to normal levels by wild‐type SOS2, but not by a mutated form of SOS2 lacking the T168 residue phosphorylated by GRIK1. Activation of SOS2 by GRIK1 was also demonstrated in a reconstituted system in yeast. Our results indicate that GRIKs phosphorylate and activate SnRK1 and other members of the SnRK3 family, and that they play important roles in multiple signalling pathways in vivo.

The battle of two ions: Ca2+ signalling against Na+ stress

“…Since GRIK kinases also regulate kinases that mediate sugar sensing, this mechanism represents a potential novel interconnection of salt stress and energy status of plants (Barajas‐Lopez et al . ).…”

“…Furthermore, it was shown that the sos2 phenotype could not be complemented by a non-phosphorylatable T168A version of SOS2. Since GRIK kinases also regulate kinases that mediate sugar sensing, this mechanism represents a potential novel interconnection of salt stress and energy status of plants ( Barajas-Lopez et al 2018).…”

AtCIPK16 Mediates Salt Stress Through Phytohormones and Transcription Factors

“…Lee et al (2007) has suggested the possibility of CBL1 and CBL9 to be the interacting partners of CIPK16. More recently, the ability of other kinases, such as GRIK kinases, to release the auto-inhibitory state of SOS2 has been established ( Barajas-Lopez et al 2018). This implies that there could be an alternative interactome for CIPKs apart from the well-known CBLs to release it from its' auto-inhibitory form.…”

“…Salt stress signals may be sensed by "sensor molecules" owing to the salt stress related changes in cytosolic Ca 2+ levels in root cells. These sensor molecules then interact with/phosphorylate AtCIPK16 to release it from the auto-inhibitory state (Barajas-Lopez et al 2018;Sanchez-Barrena et al 2007).…”

Energy costs of salinity tolerance in crop plants

“…Stoichiometries of the Na + /H + antiporters and proton pumps (H + /ATP) are critical for models of energy use, as are voltage dependences and conductances of transporters such as VisHKT1 (Henderson et al ., ). Likely interactions of the transport of Na + with K + (Nieves‐Cordones et al ., ), and Cl − with NO 3 − (Wege et al ., ; Wen et al ., ) are also important, as well as unidentified K + transporters that may be important under salinity (Caballero et al ., ). Energy costs of phosphorylation, though important in regulation of transport (Barajas‐Lopez et al ., ), are probably small (Shacter et al ., ).…”