Salt stress has a detrimental impact on food crop production, with its severity escalating due to both natural and man-made factors. As one of the most important food crops, wheat is susceptible to salt stress, resulting in abnormal plant growth and reduced yields; therefore, damage from salt stress should be of great concern. Additionally, the utilization of land in coastal areas warrants increased attention, given diminishing supplies of fresh water and arable land, and the escalating demand for wheat. A comprehensive understanding of the physiological and molecular changes in wheat under salt stress can offer insights into mitigating the adverse effects of salt stress on wheat. In this review, we summarized the genes and molecular mechanisms involved in ion transport, signal transduction, and enzyme and hormone regulation, in response to salt stress based on the physiological processes in wheat. Then, we surveyed the latest progress in improving the salt tolerance of wheat through breeding, exogenous applications, and microbial pathways. Breeding efficiency can be improved through a combination of gene editing and multiple omics techniques, which is the fundamental strategy for dealing with salt stress. Possible challenges and prospects in this process were also discussed.

Leaf senescence is an important factor affecting the functional transition from nutrient assimilation to nutrient remobilization in crops. The senescence of wheat leaves is of great significance for its yield and quality. In the leaf senescence process, transcriptional regulation is a committed step in integrating various senescence-related signals. Although the plant-specific transcriptional regulation factor valine-glutamine (VQ) gene family is known to participate in different physiological processes, its role in leaf senescence is poorly understood. We isolated TaVQ25-A and studied its function in leaf senescence regulation. TaVQ25-A was mainly expressed in the roots and leaves of wheat. The TaVQ25-A-GFP fusion protein was localized in the nuclei and cytoplasm of wheat protoplasts. A delayed senescence phenotype was observed after dark and abscisic acid (ABA) treatment in TaVQ25-A-silenced wheat plants. Conversely, overexpression of TaVQ25-A accelerated leaf senescence and led to hypersensitivity in ABA-induced leaf senescence in Arabidopsis. A WRKY type transcription factor, TaWRKY133, which is tightly related to the ABA pathway and affects the expression of some ABA-related genes, was found to interact with TaVQ25-A both in vitro and in vivo. Results of this study indicate that TaVQ25-A is a positive regulator of ABA-related leaf senescence and can be used as a candidate gene for wheat molecular breeding.

Leaves are the primary harvest portion in forage crops such as alfalfa (Medicago sativa). Delaying leaf senescence is an effective strategy to improve forage biomass production and quality. In this study, we employed transcriptome sequencing to analyze the transcriptional changes and identify key senescence-associated genes under age-dependent leaf senescence in Medicago truncatula, a legume forage model plant. Through comparing the obtained expression data at different time points, we obtained 1057 differentially expressed genes, with 108 consistently up-regulated genes across leaf growth and senescence. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses showed that the 108 SAGs mainly related to protein processing, nitrogen metabolism, amino acid metabolism, RNA degradation and plant hormone signal transduction. Among the 108 SAGs, seven transcription factors were identified in which a novel bZIP transcription factor MtbZIP60 was proved to inhibit leaf senescence. MtbZIP60 encodes a nuclear-localized protein and possesses transactivation activity. Further study demonstrated MtbZIP60 could associate with MtWRKY40, both of which exhibited an up-regulated expression pattern during leaf senescence, indicating their crucial roles in the regulation of leaf senescence. Our findings help elucidate the molecular mechanisms of leaf senescence in M. truncatula and provide candidates for the genetic improvement of forage crops, with a focus on regulating leaf senescence.

UDP-glycosyltransferases (UGTs) represent a large multigene family that play a central role in glycosylating a highly diverse array of natural products, underscoring their critical importance in various biological processes. However, the functional roles of a substantial majority of UGTs remain to be elucidated. In the present study, we characterized the glycosyltransferase UGT78G3, a member of the UGT78 glycosyltransferase family in the model legume Medicago truncatula. Amino-acid sequence analysis revealed a conserved PSPG motif at the C-terminus of UGT78G3. Liquid chromatography-coupled tandem mass spectrometry (LC-MS/MS) analysis demonstrated that UGT78G3 catalyzes the formation of kaempferol 3-O-glucoside in vitro. However, neither UGT78G3 overexpression nor CRISPR/Cas9-mediated mutagenesis resulted in significant changes to the endogenous levels of kaempferol 3-O-glucoside, indicating that UGT78G3 does not play a predominant role in the biosynthesis of kaempferol 3-O-glucoside in vivo. Our findings identify a putative glycosyltransferase in M. truncatula and provide a target for biocatalyst design aimed at synthesizing flavonoid glucosides.

Leaf senescence is a pivotal developmental program in plants, precisely regulated by diverse signals including salicylic acid (SA). The Arabidopsis VQ protein AtVQ25 has been previously characterized as a positive regulator of SA-mediated leaf senescence, functioning through interaction with AtWRKY53 to relieve the transcriptional self-repression of AtWRKY53 at its own promoter. However, the upstream regulatory mechanisms governing AtVQ25 itself remain elusive. In this study, a yeast library screening was performed, and the mitogen-activated protein kinases AtMPK1 and AtMPK2 were identified as interacting partners of AtVQ25. The direct physical interaction was validated by yeast two-hybrid (Y2H), luciferase complementation imaging (LCI), pull-down, and co-immunoprecipitation assays (Co-IP). Furthermore, AtVQ25 was shown to be directly phosphorylated by AtMPK1/AtMPK2, which enhanced its protein stability and retarded its degradation, thereby positively modulating leaf senescence progression. Genetic analyses revealed that the function of AtVQ25 in SA-mediated leaf senescence depends on the functional integrity of AtMPK1/AtMPK2. Collectively, these findings establish AtMPK1/AtMPK2 as upstream interactors of AtVQ25 that coordinate SA-mediated leaf senescence through phosphorylation-dependent enhancement of AtVQ25 protein stability, providing novel insights into the upstream regulatory circuitry of VQ proteins.