Soil salinity is a major constraint on soybean (Glycine max) production. While ionic toxicity is a primary factor, the integration of metabolic and hormonal responses remains unclear. Here, we characterize the salt-sensitive mutant, sss1, using physiological, metabolomic, and transcriptomic analyses. We demonstrate that the primary defect in sss1 is disrupted ion homeostasis, characterized by excessive Na+ accumulation, impaired K+ retention, and a high Na+/K+ ratio. Multi-omics integration revealed that sss1 exhibits extensive metabolic reprogramming. Notably, mannose was identified as a potential hub linking carbohydrate metabolism and glycosylation; its reduction in the mutant suggests a metabolic vulnerability. Furthermore, the mutant showed a dual impairment of abscisic acid (ABA) and jasmonic acid (JA) signaling, evidenced by reduced hormone levels and downregulation of biosynthetic genes. Collectively, our results associate the sss1 locus with systemic disruptions in ion homeostasis, hormone signaling, and metabolic reprogramming. This multi-omics landscape provides a foundation for the future cloning of SSS1 and elucidating the molecular mechanisms underlying salt sensitivity in soybean.
Chen et al. (Sat,) studied this question.