CRK2 enhances salt tolerance by regulating callose deposition in connection with PLDα1

Abstract High salinity has become an increasingly prevalent source of stress to which plants need to adapt. The receptor-like protein kinases (RLKs), including the cysteine-rich receptor-like kinase (CRK) subfamily, are a highly expanded family of transmembrane proteins in plants that are largely responsible for communication between cells and the extracellular environment. Various CRKs have been implicated in biotic and abiotic stress responses, however their functions on a cellular level remain largely uncharacterized. Here we have shown that CRK2 enhances salt tolerance at the germination stage in Arabidopsis thaliana and also modulates root length. We established that functional CRK2 is required for salt-induced callose deposition. In doing so, we revealed a novel role for callose deposition, in response to increased salinity, and demonstrated its importance for salt tolerance during germination. Using fluorescently tagged proteins we observed specific changes in CRK2’s subcellular localization in response to various stress treatments. Many of CRK2’s cellular functions were dependent on phospholipase D (PLD) activity, as were the subcellular localization changes. Thus we propose that CRK2 acts downstream of PLD during salt stress to promote callose deposition and regulate plasmodesmal permeability, and that CRK2 adopts specific stress-dependent subcellular localization patterns in order to carry out its functions. One sentence summaryThe receptor-like kinase CRK2 adopts PLDα1-dependent stress-induced subcellular localization patterns to regulate callose deposition at plasmodesmata, enhancing salt tolerance in Arabidopsis thaliana.