Rice lectin receptor-like kinase provides salinity tolerance by ion homeostasis.

ABSTRACT

Sensing stress and activating the downstream signaling pathways is the imperative step for stress response. Lectin receptor-like kinase (LecRLK) is an important family that plays a key role in sensing stress conditions through lectin receptor and activates downstream signaling by kinase domain. We identified the role of OsLecRLK gene for salinity stress tolerance and hypothesized its role in Na+ extrusion from cell. OsLecRLK overexpression and downregulation (through artificial miRNA) transgenic lines were developed and its comparison with wild-type (WT) plants were performed overexpression transgenic lines showed better performance, whereas downregulation showed poor performance than WT. Lower accumulation of reactive oxygen species (ROS), malondialdehyde and toxic ion, and a higher level of proline, RWC, ROS scavengers in overexpression lines lead us to the above conclusion. Based on the relative expression of stress-responsive genes, ionic content and interactome protein, working model highlights the role of OsLecRLK in the extrusion of Na+ ion from the cell. This extrusion is facilitated by a higher expression of salt overly sensitive 1 (Na+ /K+ channel) in overexpression transgenic line. Altered expression of stress-responsive genes and changed biochemical and physiological properties of cell suggests an extensive reprogramming of the stress-responsive metabolic pathways by OsLecRLK under stress condition, which could be responsible for the salt tolerance capability.