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

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.

SUBMITTER: Yu Y

PROVIDER: S-EPMC7395154 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:We investigated the effects of salt-sensitive signaling molecules on ionic fluxes and gene expression related to K+/Na+ homeostasis in a perennial herb, Glycyrrhiza uralensis, during short-term NaCl stress (100 mM, 24 h). Salt treatment caused more pronounced Na+ accumulation in root cells than in leaf cells. Na+ ions were mostly compartmentalized in vacuoles. Roots exposed to NaCl showed increased levels of extracellular ATP (eATP), cytosolic Ca2+, H2O2, and NO. Steady-state flux recordings revealed that these salt-sensitive signaling molecules enhanced NaCl-responsive Na+ efflux, due to the activated Na+/H+ antiport system in the plasma membrane (PM). Moreover, salt-elicited K+ efflux, which was mediated by depolarization-activated cation channels, was reduced with the addition of Ca2+, H2O2, NO, and eATP. The salt-adaptive effects of these molecules (Na+ extrusion and K+ maintenance) were reduced by pharmacological agents, including LaCl3 (a PM Ca2+ channel inhibitor), DMTU (a reactive oxygen species scavenger), cPTIO (an NO scavenger), or PPADS (an antagonist of animal PM purine P2 receptors). RT-qPCR data showed that the activation of the PM Na+/H+ antiport system in salinized roots most likely resulted from the upregulation of two genes, GuSOS1 and GuAHA, which encoded the PM Na+/H+ antiporter, salt overly sensitive 1 (SOS1), and H+-ATPase, respectively. Clear interactions occurred between these salt-sensitive agonists to accelerate transcription of salt-responsive signaling pathway genes in G. uralensis roots. For example, Ca2+, H2O2, NO, and eATP promoted transcription of GuSOS3 (salt overly sensitive 3) and/or GuCIPK (CBL-interacting protein kinase) to activate the predominant Ca2+-SOS signaling pathway in salinized liquorice roots. eATP, a novel player in the salt response of G. uralensis, increased the transcription of GuSOS3, GuCIPK, GuRbohD (respiratory burst oxidase homolog protein D), GuNIR (nitrate reductase), GuMAPK3, and GuMAPK6 (the mitogen-activated protein kinases 3 and 6). Moreover, GuMAPK3 and GuMAPK6 expression levels were enhanced by H2O2 in NaCl-stressed G. uralensis roots. Our results indicated that eATP triggered downstream components and interacted with Ca2+, H2O2, and NO signaling to maintain K+/Na+ homeostasis. We propose that a multiple signaling network regulated K+/Na+ homeostasis in NaCl-stressed G. uralensis roots.

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

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

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