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.

Soil salinization is an essential environmental stressor, threating agricultural yield and ecological security worldwide. Saline soils accumulate excessive soluble salts which are detrimental to most plants by limiting plant growth and productivity. It is of great necessity for plants to efficiently deal with the adverse effects caused by salt stress for survival and successful reproduction. Multiple determinants of salt tolerance have been identified in plants, and the cellular and physiological mechanisms of plant salt response and adaption have been intensely characterized. Plants respond to salt stress signals and rapidly initiate signaling pathways to re-establish cellular homeostasis with adjusted growth and cellular metabolism. This review summarizes the advances in salt stress perception, signaling and response in plants. A better understanding of plant salt resistance will contribute to improving crop performance under saline conditions using multiple engineering approaches. The rhizosphere microbiome-mediated plant salt tolerance as well as chemical priming for enhanced plant salt resistance are also discussed in this review.

Salt stress is one of the significant environmental stressors that severely affects plant growth and development. Plant responses to salt stress involve a series of biological mechanisms, including osmoregulation, redox and ionic homeostasis regulation, as well as hormone or light signaling-mediated growth adjustment, which are regulated by different functional components. Unraveling these adaptive mechanisms and identifying the critical genes involved in salt response and adaption are crucial for developing salt-tolerant cultivars. This review summarizes the current research progress in the regulatory networks for plant salt tolerance, highlighting the mechanisms of salt stress perception, signaling, and tolerance response. Finally, we also discuss the possible contribution of microbiota and nanobiotechnology to plant salt tolerance.

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. Drought stress is a key environmental factor that severely reduces crop yield all over the world. The phytohormone abscisic acid (ABA) is known to mediate drought responses through regulating drought-responsive genes expression and stomatal closure, but the mechanisms that negatively regulate this process and prevent the adverse effects of excess drought responses on plant growth is less well studied. Here, we show that a HD-ZIP II transcription factor HAT1 negatively regulates ABA-mediated drought responses through suppressing ABA biosynthesis and signaling. The hat1hat3 mutant showed ABA-hypersensitive and drought-tolerant phenotypes, whereas the HAT1-overexpressing lines were insensitive to ABA and less tolerant to drought. Furthermore, we found SnRK2.3 kinase, a positive component of ABA signaling, interacts with and phosphorylates HAT1 to destabilize and suppress its binding activity. Overexpression of SnRK2.3 reduces HAT1 protein level and inhibits HAT1OX phenotypes in ABA and drought responses. Our results revealed a HAT1-mediated negative regulatory mechanism in attenuating the ABA signaling and drought response.