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(2+)-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.