Arabidopsis P4 ATPase-mediated cell detoxification confers resistance to Fusarium graminearum and Verticillium dahliae

Toxic metabolites produced by phytopathogens can subvert host immunity. Here the authors show that the Arabidopsis P4-ATPases, AtALA1 and AtALA7 mediate mycotoxin detoxification by promoting vesicle transport and their subsequent sequestration and degradation in vacuoles. Many toxic secondary metabolites produced by phytopathogens can subvert host immunity, and some of them are recognized as pathogenicity factors. Fusarium head blight and Verticillium wilt are destructive plant diseases worldwide. Using toxins produced by the causal fungi Fusarium graminearum and Verticillium dahliae as screening agents, here we show that the Arabidopsis P4 ATPases AtALA1 and AtALA7 are responsible for cellular detoxification of mycotoxins. Through AtALA1-/AtALA7-mediated vesicle transport, toxins are sequestered in vacuoles for degradation. Overexpression of AtALA1 and AtALA7 significantly increases the resistance of transgenic plants to F. graminearum and V. dahliae, respectively. Notably, the concentration of deoxynivalenol, a mycotoxin harmful to the health of humans and animals, was decreased in transgenic Arabidopsis siliques and maize seeds. This vesicle-mediated cell detoxification process provides a strategy to increase plant resistance against different toxin-associated diseases and to reduce the mycotoxin contamination in food and feed.

Automated summary

The Arabidopsis P4-ATPases AtALA1 and AtALA7 are found to detoxify mycotoxins by promoting vesicle transport, leading to their sequestration and degradation in vacuoles. Overexpression of AtALA1 and AtALA7 enhances plant resistance to Fusarium graminearum and Verticillium dahliae, while reducing the concentration of harmful mycotoxins in Arabidopsis siliques and maize seeds. This vesicle-mediated cell detoxification process offers a strategy to boost plant resistance against toxin-associated diseases and lower mycotoxin contamination in food and feed.