Salt stress is a major environmental stress that affects plant growth and development. Plants are sessile and thus have to develop suitable mechanisms to adapt to high-salt environments. Salt stress increases the intracellular osmotic pressure and can cause the accumulation of sodium to toxic levels. Thus, in response to salt stress signals, plants adapt via various mechanisms, including regulating ion homeostasis, activating the osmotic stress pathway, mediating plant hormone signaling, and regulating cytoskeleton dynamics and the cell wall composition. Unraveling the mechanisms underlying these physiological and biochemical responses to salt stress could provide valuable strategies to improve agricultural crop yields. In this review, we summarize recent developments in our understanding of the regulation of plant salt stress.

The Salt Overly Sensitive (SOS) pathway regulates intracellular sodium ion (Na+) homeostasis and salt tolerance in plants. Until recently, little was known about the mechanisms that inhibit the SOS pathway when plants are grown in the absence of salt stress. In this study, we report that the Arabidopsis thaliana 14-3-3 proteins λ and κ interact with SOS2 and repress its kinase activity. Growth in the presence of salt decreases the interaction between SOS2 and the 14-3-3 proteins, leading to kinase activation in planta. 14-3-3 λ interacts with the SOS2 junction domain, which is important for its kinase activity. A phosphorylation site (Ser-294) is identified within this domain by mass spectrometry. Mutation of Ser-294 to Ala or Asp does not affect SOS2 kinase activity in the absence of the 14-3-3 proteins. However, in the presence of 14-3-3 proteins, the inhibition of SOS2 activity is decreased by the Ser-to-Ala mutation and enhanced by the Ser-to-Asp exchange. These results identify 14-3-3 λ and κ as important regulators of salt tolerance. The inhibition of SOS2 mediated by the binding of 14-3-3 proteins represents a novel mechanism that confers basal repression of the SOS pathway in the absence of salt stress.

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Drought is a major threat to plant growth and crop productivity. The phytohormone abscisic acid (ABA) plays a critical role in plant response to drought stress. Although ABA signaling-mediated drought tolerance has been widely investigated in Arabidopsis thaliana, the feedback mechanism and components negatively regulating this pathway are less well understood. Here we identified a member of Arabidopsis HD-ZIP transcription factors HAT1 which can interacts with and be phosphorylated by SnRK2s. hat1hat3, loss-of-function mutant of HAT1 and its homolog HAT3, was hypersensitive to ABA in primary root inhibition, ABA-responsive genes expression, and displayed enhanced drought tolerance, whereas HAT1 overexpressing lines were hyposensitive to ABA and less tolerant to drought stress, suggesting that HAT1 functions as a negative regulator in ABA signaling-mediated drought response. Furthermore, expression levels of ABA biosynthesis genes ABA3 and NCED3 were repressed by HAT1 directly binding to their promoters, resulting in the ABA level was increased in hat1hat3 and reduced in HAT1OX lines. Further evidence showed that both protein stability and binding activity of HAT1 was repressed by SnRK2.3 phosphorylation. Overexpressing SnRK2.3 in HAT1OX transgenic plant made a reduced HAT1 protein level and suppressed the HAT1OX phenotypes in ABA and drought response. Our results thus establish a new negative regulation mechanism of HAT1 which helps plants fine-tune their drought responses.

As abscisic acid (ABA) receptors, PYR1/PYL/RCAR (PYLs) play important roles in ABA-mediated seed germination, but the regulation of PYLs in this process, especially at the transcriptional level, remains unclear. In this study, we found that expression of 11 of 14 PYLs changes significantly during seed germination and is affected by exogenous ABA. Two PYLs, PYL11 and PYL12, both of which are expressed specifically in mature seeds, positively modulate ABA-mediated seed germination. However, ABI5 was found to modulate the PYL11-and PYL12-mediated ABA response. In the abi5-7 mutant, ABA hypersensitivity caused by PYL11 and PYL12 overexpression was totally or partially blocked. By contrast, ABI5 regulates the expression of PYL11 and PYL12 by directly binding to their promoters. Moreover, the expression of eight other PYLs is also affected during the germination of abi5 mutants. Promoter analysis revealed that an ABI5binding region is present next to the TATA box or initiator box. Together, our data demonstrate the role of PYL11 and PYL12 in seed germination. In addition, the identification of PYLs as targets of ABI5 reveals a role of ABI5 in the feedback regulation of ABA-mediated seed germination.