Overexpression of phosphatidylserine synthase IbPSS1 affords cellular Na+ homeostasis and salt tolerance by activating plasma membrane Na+/H+ antiport activity in sweet potato roots

Yicheng Yu,Zhonghou Tang,Jian Sun,Zhiyuan Pan,Lei Zhang,Meng Kou,Xiaofeng Bian,Zongyun Li,Qinghe Cao,Daifu Ma,Ying Xuan,Qiang Li

doi:10.1038/s41438-020-00358-1

Yicheng Yu, Zhonghou Tang + Show 10 more

Open Access

https://doi.org/10.1038/s41438-020-00358-1

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Abstract

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 IbPSS1 gene, which encodes an ortholog of Arabidopsis AtPSS1, from sweet potato (Ipomoea batatas (L.) Lam.). The transient expression of IbPSS1 in Nicotiana benthamiana leaves increased PS abundance. We then established an efficient Agrobacterium rhizogenes-mediated in vivo root transgenic system for sweet potato. Overexpression of IbPSS1 through this system markedly decreased cellular Na+ accumulation in salinized transgenic roots (TRs) compared with adventitious roots. The overexpression of IbPSS1 enhanced salt-induced Na+/H+ antiport activity and increased plasma membrane (PM) Ca2+-permeable channel sensitivity to NaCl and H2O2 in the TRs. We confirmed the important role of IbPSS1 in improving salt tolerance in transgenic sweet potato lines obtained from an Agrobacterium tumefaciens-mediated transformation system. Similarly, compared with the wild-type (WT) plants, the transgenic lines presented decreased Na+ accumulation, enhanced Na+ exclusion, and increased PM Ca2+-permeable channel sensitivity to NaCl and H2O2 in the roots. Exogenous application of lysophosphatidylserine triggered similar shifts in Na+ accumulation and Na+ and Ca2+ 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 IbPSS1 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 Ca2+ signaling in the roots.

Highlights

Introduction High concentrations ofNaCl in the soil disrupt plant growth, cellular K+/Na+ homeostasis, and metabolic processes and markedly decrease crop yield in irrigated lands[1]
Our results revealed that IbPSS1 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 Ca2+ signaling in the roots
To confirm whether IbPSS1 contributes to PS synthesis, we transiently coexpressed IbPSS1 with a genetically encoded biosensor of PS (C2LACT-GFP) in Nicotiana benthamiana leaves

Summary

Introduction

NaCl in the soil disrupt plant growth, cellular K+/Na+ homeostasis, and metabolic processes and markedly decrease crop yield in irrigated lands[1]. Many plants activate plasma membrane (PM) Na+/H+ antiporter-mediated Na+ exclusion to maintain Na+ homeostasis in the cytosol under saline conditions[1,2]. The conserved salt overly sensitive (SOS) pathway regulates PM Na+/H+. Antiporter activation in plants; in this pathway, a saltinduced buildup of cytosolic Ca2+ ([Ca2+]cyt) is identified by SOS3/CBL4 calcium sensors, which bind to SOS2/. CIPK24 to form a complex[2]. The SOS2–SOS3 complex phosphorylates SOS1/NHX7 (a PM Na+/H+ antiporter), which can export Na+ from the cell[2]. Salt stress rapidly triggers an apoplastic H2O2 burst, which promotes the mediation of Na+ homeostasis in various plant species[3,4,5].

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