SlSLAH2 mediates malate exudation and contributes to aluminum tolerance

Abstract

Abstract Malate transporters play pivotal roles in plant aluminum tolerance mechanisms. In the classic aluminum tolerance pathway, Al 3+ induces ALMT , which promotes malate exudation to chelate Al 3+ to enhance aluminum tolerance. However, in tomato, SlALMT was inhibited by Al 3+ , but Al 3+ still induced malate exudation. We found that SlSLAH2, upon induction by Al 3+ , can transport malate and is required for full activation of malate exudation by Al 3+ stress. SlWRKY37 contributes to SlSLAH2 induction by Al 3+ . Moreover, SlSLAH2 is phosphorylated in response to Al 3+ . 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, Al 3+ downregulated SlPP2C72 , and Al 3+ treated seedling extracts can suppress SlPP2C72 phosphatase activity. We propose a synergistic transcription-phosphorylation cascade that can ensure a robust malate exudation across Al 3+ environments.