SlSLAH2 mediates malate exudation and contributes to aluminum tolerance.

Abstract

Malate transporters play pivotal roles in plant aluminum tolerance mechanisms. In the classic aluminum tolerance pathway, Al³⁺ induces ALMT, which promotes malate exudation to chelate Al³⁺ to enhance aluminum tolerance. However, in tomato, SlALMT was inhibited by Al³⁺, but Al³⁺ still induced malate exudation. We found that SlSLAH2, upon induction by Al³⁺, can transport malate and is required for full activation of malate exudation by Al³⁺ stress. SlWRKY37 contributes to SlSLAH2 induction by Al³⁺. Moreover, SlSLAH2 is phosphorylated in response to Al³⁺. We identify SlCDPK21 and SlPP2C72 as putative upstream kinase and phosphatase that could potentially facilitate phosphorylation homeostasis. SlCDPK21 can interact with SlSLAH2 in a heterologous system, phosphorylate SlSLAH2 at Thr167 in vitro and is also required for full malate exudation. SlPP2C72 can dephosphorylate SlSLAH2 in vitro and knock-out leads to increased malate exudation. Furthermore, Al³⁺ downregulated SlPP2C72, and Al³⁺ treated seedling extracts can suppress SlPP2C72 phosphatase activity. We propose a synergistic transcription-phosphorylation cascade that can ensure a robust malate exudation across Al³⁺ environments.