Phosphate-induced resistance to pathogen infection in Arabidopsis

SUMMARY In nature, plants are concurrently exposed to a number of abiotic and biotic stresses. Our understanding of convergence points between responses to combined biotic/abiotic stress pathways remains, however, rudimentary. Here we show that MIR399 overexpression, loss-of-function of PHO2 ( PHOSPHATE2 ), or treatment with high Pi, is accompanied by an increase in phosphate (Pi) content and accumulation of reactive oxygen species (ROS) in Arabidopsis thaliana . High Pi plants (e.g. miR399 overexpressor, pho2 mutant, and plants grown under high Pi supply) exhibited resistance to infection by necrotrophic and hemibiotrophic fungal pathogens. In the absence of pathogen infection, the expression level of genes in the salicylic acid (SA)- and jasmonic acid (JA)-dependent signaling pathways was higher in high Pi plants compared to wild type plants, which is consistent with increased levels of SA and JA in non-infected high Pi plants. During infection, an opposite regulation in the two branches of the JA pathway (ERF1/PDF1.2 and MYC2/VSP2) occurs in high Pi plants. Thus, while the ERF1-PDF1 branch positively responds to fungal infection, the MYC2/VSP2 branch is negatively regulated during pathogen infection in high Pi plants. This study supports that Pi accumulation promotes resistance to infection by fungal pathogens in Arabidopsis, while providing a basis to better understand crosstalk between Pi signaling and hormonal signalling pathways for modulation of plant immune responses. Significance statement This study highlights the importance of phosphate (Pi) in regulating immune responses, hence, disease resistance in Arabidopsis thaliana . Increasing Pi content either by MIR399 overexpression (or loss-of-function of PHOSPHATE2 ), as well as by Pi treatment enhances resistance to infection by necrotrophic and hemibiotrophic fungal pathogens through modulation of SA- and JA-dependent signaling pathways. These results also support that miR399 functions as a regulator of Arabidopsis immunity.