The <scp>E3</scp> ubiquitin ligase <scp>SCF^EDL3</scp> mediates salt stress response by degradation of <scp>IbPP2CA2</scp> to regulate <scp>ABA</scp> signaling in sweetpotato

The phytohormone abscisic acid (ABA) plays a critical role as a signaling molecule, mediating adaptive responses of plants to salt stress. However, the orchestration of ABA signaling in response to salt stress in sweetpotato remains poorly understood. In this study, we cloned a gene of unknown function, IbEDL3, which is significantly upregulated in sweetpotato under salt stress conditions. Transgenic sweetpotato plants overexpressing IbEDL3 exhibited enhanced proline accumulation, reaction oxygen species (ROS) scavenging, stomatal closure, and Na⁺ efflux compared with wild-type (WT) plants under salt stress. Further investigation revealed that IbEDL3 interacts with IbSKP1-1, forming part of the E3 ubiquitin ligase SCF^EDL3 complex. Although IbEDL3 interacted with IbABI1, IbABI2, and IbPP2CA2, the SCF^EDL3 complex only ubiquitinated and degraded IbPP2CA2. Under salt stress, SCF^EDL3 accelerated the ubiquitination and degradation of IbPP2CA2, leading to the release of more IbSnRK2.6, which further promoted ABA signaling to regulate stomatal closure, proline accumulation and Na⁺ efflux. Inhibition of IbPP2CA2 resulted in enhanced salt tolerance in sweetpotato. Collectively, the SCF^IbEDL3-IbPP2CA2 module provides insight into the mechanisms underlying ABA signaling in response to salt stress and offers a new avenue for genetic improvement of salt tolerance in sweetpotato.