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For plant growth under salt stress, sensing and transducing salt signals are central to cellular Na+ homoeostasis. The calcineurin B‐like protein (CBL)‐CBL‐interacting protein kinase (CIPK) complexes play critical roles in transducing salt signals in plants. Here, we show that CBL5, an ortholog of CBL4 and CBL10 in Arabidopsis, interacts with and recruits CIPK8/CIPK24 to the plasma membrane. Yeast cells coexpressing CBL5, CIPK8/CIPK24 and SOS1 demonstrated lesser Na+ accumulation and a better growth phenotype than the untransformed or SOS1 transgenic yeast cells under salinity. Overexpression of CBL5 improved the growth of the cipk8 or cipk24 single mutant but not the cipk8 cipk24 double mutant under salt stress, suggesting that CIPK8 and CIPK24 were the downstream targets of CBL5. Interestingly, seed germination in cbl5 was severely inhibited by NaCl, which was recovered by the overexpression of CBL5. Furthermore, CBL5 was mainly expressed in the cotyledons and hypocotyls, which are essential to seed germination. Na+ efflux activity in the hypocotyls of cbl5 was reduced relative to the wild‐type under salt stress, enhancing Na+ accumulation. These findings indicate that CBL5 functions in seed germination and protects seeds and germinating seedlings from salt stress through the CBL5‐CIPK8/CIPK24‐SOS1 pathways. Summary statement: Perceiving and transducing salt signals are critical to cellular Na+ homoeostasis for plant growth under salt stress. This article finds that calcineurin B‐like (CBL5) interacts with CIPK8/CIPK24 to activate SOS1 activity. The CBL5‐CIPK8/CIPK24‐SOS1 pathways may function in transducing salt signals in seed germination in Arabidopsis. [ABSTRACT FROM AUTHOR]

Salt tolerance in plants is mediated by Na+ extrusion from the cytosol by the plasma membrane Na+/H+ antiporter SOS1. This is activated in Arabidopsis root by the protein kinase complex SOS2–SOS3 and in Arabidopsis shoot by the protein kinase complex CBL10–SOS2, with SOS2 as a key node in the two pathways. The sos1 mutant is more sensitive than the sos2 mutant, suggesting that other partners may positively regulate SOS1 activity. Arabidopsis has 26 CIPK family proteins of which CIPK8 is the closest homolog to SOS2. It is hypothesized that CIPK8 can activate Na+ extrusion by SOS1 similarly to SOS2. The plasma membrane Na+/H+ exchange activity of transgenic yeast co-expressing CBL10 , CIPK8 , and SOS1 was higher than that of untransformed and SOS1 transgenic yeast, resulting in a lower Na+ accumulation and a better growth phenotype under salinity. However, CIPK8 could not interact with SOS3, and the co-expression of SOS3 , CIPK8 , and SOS1 in yeast did not confer a significant salt tolerance phenotype relative to SOS1 transgenic yeast. Interestingly, cipk8 displayed a slower Na+ efflux, a higher Na+ level, and a more sensitive phenotype than wild-type Arabidopsis, but grew better than sos2 under salinity stress. As expected, sos2cipk8 exhibited a more severe salt damage phenotype relative to cipk8 or sos2. Overexpression of CIPK8 in both cipk8 and sos2cipk8 attenuated the salt sensitivity phenotype. These results suggest that CIPK8-mediated activation of SOS1 is CBL10-dependent and SOS3-independent, indicating that CIPK8 and SOS2 activity in shoots is sufficient for regulating Arabidopsis salt tolerance. [ABSTRACT FROM AUTHOR]

The plasma membrane (PM) Na+/H+ antiporter SOS1 (salt overly sensitive 1) has emerged as a key factor in regulating plant salt tolerance. The SpSOS1 gene, which encodes a PM Na+/H+ antiporter, was cloned from the halophyte Sesuvium portulacastrum and transformed into Arabidopsis sos1 mutant plants. As shown from the results, the SpSOS1 expression complemented the salt sensitivity of the sos1 mutant plants. Upon salinity stress, SpSOS1-transgenic Arabidopsis sos1 mutant seeds displayed higher germination ratio compared to the sos1 mutant. The sos1 mutant plants expressing SpSOS1 grew better and had a lower Na+/K+ ratio than that of the sos1 mutant and wild-type (WT) plants when they were treated with NaCl. In addition, SpSOS1-overexpressed Arabidopsis accumulated less malondialdehyde (MDA) and had a lower level of electrolyte leakage than that in the sos1 mutant and WT plants under salt stress. Furthermore, the SpSOS1 expression in transgenic sos1 mutant plants also increased the transcript levels of some salt stress-related genes, such as AtHKT1;1 (high-affinity K+ transporter 1;1), AtSOS2 (salt overly sensitive 2), AtSCABP8 (SOS3-like calcium binding protein 8), and AtNHX1 (Na+/H+ exchanger 1). These results suggested that SpSOS1 improved the plant salt tolerance by regulating ion homeostasis and protecting the plasma membrane against oxidative damage under salt stress. [ABSTRACT FROM AUTHOR]

The plant Na+/H+ antiporter (NHX) plays a significant role in cellular ion homeostasis. Herein, an Na+/H+ antiporter gene, SpNHX1 from the Sesuvium portulacastrum plant, was obtained by homology-cloning method. The SpNHX1 gene contains 2113 bp with an open-reading frame encoding a polypeptide of 554 amino acid residues with an estimated molecular mass of 61.27 kDa and an isoelectric point of 7.24. The amino acid sequences of SpNHX1 shared a high similarity with Arabidopsis thaliana AtNHX1 (75.81%), AtNHX2 (77.12%) and Oryza sativa OsNHX1 (73.10%). SpNHX1 contains an amiloride-binding region (FFIYLLPPI), which is a highly-conserved domain in plant Na+/H+ antiporters. RT-PCR (reverse transcriptional PCR) analysis showed that the SpNHX1 gene had a high expression level in roots compared to other tissues under normal conditions. The qRT-PCR (quantitative real-time PCR) results indicated that NaCl treatment induced the expression of SpNHX1 gene in the roots, but its transcriptional levels were not influenced by the ABA, PEG, H2O2, heat (42 °C) or cold (4 °C) stresses. The growth of yeast cells expressing SpNHX1 was better than the non-transgenic control cells in the presence of 30 mM NaCl, 0.4 M KCl, or 0.5 mM LiCl. Furthermore, transgenic yeast cells with SpNHX1 accumulated more Na+ relative to control cells under salinity stress. These results suggested that SpNHX1 was a key determinant in the salt-stress response in Sesuvium portulacastrum. [ABSTRACT FROM AUTHOR]

Wheat SOS1 (TaSOS1) activity could be relieved upon deletion of the C-terminal 168 residues (the auto-inhibitory domain). This truncated form of wheat SOS1 (TaSOS1-974) was shown to increase compensation (compared to wild-type TaSOS1) for the salt sensitivity of a yeast mutant strain, AXT3K, via increased Na + transportation out of cells during salinity stress. Expression of the plasma membrane proteins TaSOS1-974 or TaSOS1 improved the growth of transgenic tobacco plants compared with wild-type plants under normal conditions. However, plants expressing TaSOS1-974 grew better than TaSOS1-transformed plants. Upon salinity stress, Na + efflux and K + influx rates in the roots of transgenic plants expressing TaSOS1-974 or TaSOS1 were greater than those of wild-type plants. Furthermore, compared to TaSOS1-transgenic plants, TaSOS1-974-expressing roots showed faster Na + efflux and K + influx, resulting in less Na + and more K + accumulation in TaSOS1-974-transgenic plants compared to TaSOS1-transgenic and wild-type plants. TaSOS1-974-expressing plants had the lowest MDA content and electrolyte leakage among all tested plants, indicating that TaSOS1-974 might protect the plasma membrane against oxidative damage generated by salt stress. Overall, TaSOS1-974 conferred higher salt tolerance in transgenic plants compared to TaSOS1. Consistent with this result, transgenic plants expressing TaSOS1-974 showed a better growth performance than TaSOS1-expressing and wild-type plants under saline conditions., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)