AN ARABIDOPSIS PURPLE ACID PHOSPHATASE5 (PAP5) IS ESSENTIAL FOR MAINTAINING BASAL RESISTANCE AGAINST PSEUDOMONAS SYRINGAE

Abstract

Plants have evolved an array of constitutive and inducible defense strategies to restrict pathogen ingress. Despite this, some pathogens still invade plants and impair growth and productivity. Previous studies have revealed key regulators of defense responses, and efforts have been made to develop disease resistant crop plants. These attempts are hampered by the complexity of defense signaling pathways. To further elucidate the complexity of defense responses, a population of T-DNA mutants in Colombia-0 background were screened for altered defense responses to virulent Pseudomonas syringae pv. tomato DC3000 (Pst DC3000). This study demonstrated that the Arabidopsis Purple Acid Phosphatse5 (PAP5) gene, normally induced only under prolonged phosphate (Pi) starvation, was required for maintaining basal resistance to certain pathogens. The expression of PAP5 was distinctly induced only under prolonged Pi starvation and during the early stages of Pst DC3000 infection (6 h.p.i). T-DNA tagged mutant, pap5 displayed enhanced susceptibility to the virulent bacterial pathogen Pst DC3000. The PAP5 mutation greatly reduced the expression of the pathogen inducible gene PR1, compared to wild-type plants. Other defense related genes, including ICS1 and PDF1.2, were impaired in pap5 plants. Similarly, overexpression of PAP5 impaired PR1, ICS1 expression and salicylic acid (SA) accumulation. Moreover, application of benzothiodiazole (BTH), an analog of SA restored PR1 expression in pap5 plants. These results provide evidence that PAP5 acts upstream of SA accumulation to regulate the expression of other defense responsive genes. Optimal levels of PAP5 are crucial for mounting complete basal resistance. SA accumulation in transgenic plants (35S:PAP5), following Pst DC3000 infection, was only ~ 60% of the wild-type plants. PAP5 was also found to be peroxisomal localized and aid the generation of reactive oxygen species for activation of defense responses. These results suggest that optimal levels of PAP5 are required for induction of PR genes and SA accumulation, demonstrating the requirement of PAP5 for maintaining basal resistance against Pst DC3000.