Salt stress poses a significant challenge to plant growth and restricts agricultural development. To delve into the intricate mechanisms involved in soybean’s response to salt stress and find targets to improve the salt resistance of soybean, this study integrated transcriptomic, proteomic, and metabolomic analyses to explore the regulatory networks involved in soybean salt tolerance. Transcriptomic analysis revealed significant changes in transcription factors, hormone-related groups, and calcium ion signaling. Notably, the biosynthetic pathways of cutin, suberine, and wax biosynthesis play an important role in this process. Proteomic results indicated salt-induced DNA methylation and the enrichment of phosphopyruvate hydrase post-salt stress, as well as its interaction with enzymes from various metabolic pathways. Metabolomic data unveiled the synthesis of various metabolites, including lipids and flavonoids, in soybean following salt stress. Furthermore, the integrated multiomics results highlighted the activation of multiple metabolic pathways in soybean in response to salt stress, with six pathways standing out prominently: stilbenoid, diarylheptanoid, and gingerol biosynthesis; carotenoid biosynthesis; carbon fixation in photosynthetic organisms; alanine, aspartate, and glutamate metabolism; thiamine metabolism; and pyruvate metabolism. These findings not only offer valuable insights into leveraging multiomics profiling techniques for uncovering salt tolerance mechanisms but also identify candidate genes for soybean improvement.

Soil salinization poses a significant threat to global agricultural productivity. Among crops, soybean (Glycine max), an important source of oil and protein, is more susceptible to salt stress compared to other major crops such as wheat (Triticum aestivum) and rice (Oryza sativa). To better utilize saline land resources, understanding the mechanisms underlying salt tolerance in soybean is essential for developing new salt-tolerant soybean varieties that contribute to food security. This review synthesizes current knowledge on the molecular mechanisms of salt tolerance in soybean, with a focus on ion homeostasis, osmotic adjustment, oxidative balance restoration, structural adaptations, and transcriptional regulatory networks. Key findings highlight the critical roles of ion transporters—such as GmNHX1, GmSOS1, GmHKT1, and GmCLC1—in maintaining Na⁺/K⁺ and Cl⁻ balance; the accumulation of osmoprotectants like proline and LEA proteins to alleviate osmotic stress; and the activation of antioxidant systems—including SOD, CAT, and APX—to scavenge reactive oxygen species (ROS). Additionally, structural adaptations, such as salt gland-like features observed in wild soybean (Glycine soja), and transcriptional regulation via ABA-dependent and independent pathways (e.g., GmDREB, GmbZIP132, GmNAC) further enhance tolerance. Despite these advances, critical gaps remain regarding Cl⁻ transport mechanisms, rhizosphere microbial interactions, and the genetic basis of natural variation in salt tolerance. Future research should integrate genomic tools, omics-based breeding, genome editing techniques such as CRISPR-Cas9, microbial technologies, and traditional breeding methods to develop salt-tolerant soybean varieties, providing sustainable solutions for the utilization of saline–alkali soils and enhancing global food security.

MUTE functions as a pivotal transcription factor that governs the transition from self-renewal to differentiation in meristemoids during stomatal development. This transition requires MUTE expression to reach a critical threshold, yet the mechanisms that maintain its expression homeostasis remain unclear. Here, we show that the Mediator CDK8 kinase module (CKM) acts as a transcriptional coactivator of the MUTE-ICE1/SCRM2 complex to regulate meristemoid fate. Specifically, CKM cooperates with MUTE-ICE1/SCRM2 to promote the transcription of the auxin-responsive genes, such as SAUR52 and SAUR53, thereby enhancing local auxin response in meristemoids. AUXIN RESPONSE FACTORs (ARFs), including ARF6, ARF7, and ARF19, then bind to MUTE promoter and contribute to its transcription, establishing a positive feedback loop. Disruption of CKM or MUTE-ICE1/SCRM2 components reduces SAUR52/53 expression and auxin responses, leading to decreased MUTE transcription, excessive meristemoid self-renewal divisions and arrested differentiation. These defects can be partially rescued by exogenous auxin application or by overexpression of SAUR53 in the mutants. Together, our results uncover a self-reinforcing transcriptional-auxin circuit in which CKM-assisted MUTE-ICE1/SCRM2 amplifies auxin response, and auxin reciprocally sustains MUTE expression. This feedback mechanism ensures that MUTE reaches the threshold required to terminate meristemoid self-renewal and initiate differentiation, revealing how transcriptional regulation and hormone signaling are integrated to control stem cell-like behaviors during tissue patterning.