GmAKT1-mediated K absorption positively modulates soybean salt tolerance by GmCBL9-GmCIPK6 complex.

Soybean is one of the most important crops in the world. However, salt stress poses a major challenge to soybean growth and productivity. Therefore, unravelling the complex mechanisms governing salt tolerance in soybean is imperative for molecular breeding of salt-tolerant varieties to improve yield. Maintaining intracellular Na/K homeostasis is one of the key factors for plant salt tolerance. Although some salt tolerance mechanisms involving Na exclusion have been well identified in plants, few studies have been conducted on how K influx controls soybean salt tolerance. Here, we characterized the function of soybean K channel gene GmAKT1 and identified GmCBL9-GmCIPK6 complex, which modulated GmAKT1-mediated K uptake under salt stress. Functional studies found that soybean lines GmAKT1 overexpressing increased K content and promoted salt tolerance, while CRISPR/Cas9-mediated disruption of GmAKT1 soybean lines decreased the K content and showed salt sensitivity. Furthermore, we identified that GmCIPK6 interacted with GmAKT1 and GmCBL9 interacted with GmCIPK6. In addition, Mn-Phos-tag assays proved that GmCIPK6 could phosphorylate GmAKT1. This collaborative activation of the GmCBL9-GmCIPK6-GmAKT1 module promoted K influx and enhanced soybean salt tolerance. Our findings reveal a new molecular mechanism in soybeans under salt stress and provide insights for cultivating new salt-tolerant soybean varieties by molecular breeding.