PaLectinL7 enhances salt tolerance of sweet cherry by regulating lignin deposition in connection with PaCAD1.

Lectin receptor-like kinases (LecRLKs), a large family of plant receptor-like kinases, play an important role in plant response to abiotic stresses. However, little information is available about the roles of LecRLKs in the salt stress response of sweet cherry (Prunus avium). Here, an L-type LecRLK gene (PaLectinL7) was characterized from sweet cherry. Subcellular localization analysis revealed that PaLectinL7 is a plasma membrane protein. The expression of PaLectinL7 was up-regulated by salt, drought and exogenously gibberellin treatments. Overexpression of PaLectinL7 in the roots of Gisela 6 enhanced its tolerance to salt stress. Additionally, transcriptome analysis showed that lignin metabolic-related genes were regulated by PaLectinL7 overexpression. Meanwhile, the lignin contents and associated enzymes (CAD and COMT) rose concurrently with PaLectinL7 overexpression under salt stress. We also found that PaCAD1, a key enzyme involved in lignin metabolism, interacted with PaLectinL7 and could be phosphorylated by PaLectinL7 in vitro, suggesting that PaLectinL7 may regulate the enzyme activity of PaCAD1. Therefore, these results indicated that PaLectinL7, as a membrane-bound regulator, promoted lignin deposition by regulating the activities of enzymes related to lignin metabolism, thus enhancing salt tolerance.