Overexpression of phosphatidylserine synthase affords cellular Na homeostasis and salt tolerance by activating plasma membrane Na/H antiport activity in sweet potato roots.

Phosphatidylserine synthase (PSS)-mediated phosphatidylserine (PS) synthesis is crucial for plant development. However, little is known about the contribution of PSS to Na homeostasis regulation and salt tolerance in plants. Here, we cloned the gene, which encodes an ortholog of , from sweet potato ( (L.) Lam.). The transient expression of in leaves increased PS abundance. We then established an efficient -mediated in vivo root transgenic system for sweet potato. Overexpression of through this system markedly decreased cellular Na accumulation in salinized transgenic roots (TRs) compared with adventitious roots. The overexpression of enhanced salt-induced Na/H antiport activity and increased plasma membrane (PM) Ca-permeable channel sensitivity to NaCl and HO in the TRs. We confirmed the important role of in improving salt tolerance in transgenic sweet potato lines obtained from an -mediated transformation system. Similarly, compared with the wild-type (WT) plants, the transgenic lines presented decreased Na accumulation, enhanced Na exclusion, and increased PM Ca-permeable channel sensitivity to NaCl and HO in the roots. Exogenous application of lysophosphatidylserine triggered similar shifts in Na accumulation and Na and Ca fluxes in the salinized roots of WT. Overall, this study provides an efficient and reliable transgenic method for functional genomic studies of sweet potato. Our results revealed that contributes to the salt tolerance of sweet potato by enabling Na homeostasis and Na exclusion in the roots, and the latter process is possibly controlled by PS reinforcing Ca signaling in the roots.