Inositol hexakisphosphate biosynthesis underpins PAMP-triggered immunity to Pseudomonas syringae pv. tomato in Arabidopsis thaliana but is dispensable for establishment of systemic acquired resistance

Abstract

Phytic acid (inositol hexakisphosphate, InsP6) is an important phosphate store and signal molecule necessary for maintenance of basal resistance to plant pathogens. Arabidopsis thaliana (L.) Heynh. ('arabidopsis') has three genes encoding myo-inositol phosphate synthases (IPS1–3), the enzymes that catalyse conversion of glucose-6-phosphate to InsP, the first step in InsP6 biosynthesis. There is one gene for inositol-(1,3,4,5,6)-pentakisphosphate 2-kinase (IPK1), which catalyzes the final step. Previously, we showed that mutation of IPS2 and IPK1 but not IPS1 increased susceptibility to pathogens. Our aim was to better understand the InsP6 biosynthesis pathway in plant defence. Here we found that the susceptibility of arabidopsis (Col-0) to virulent and avirulent Pseu-domonas syringae pv. tomato was also increased in ips3 and ips2/3 double mutants. Also, ipk1 plants had compromised expression of local acquired resistance induced by treatment with the pathogen-derived molecular pattern (PAMP) molecule flg22, but were unaffected in other responses to flg22, including Ca2+ influx and the oxidative burst, seed-ling root growth inhibition, and transcriptional up-regulation of the PAMP-triggered genes MITOGEN-ACTIVATED PROTEIN KINASE (MPK) 3, MPK11, CINNAMYL ALCOHOL DEHYDROGENASE 5, and FLG22-INDUCED RECEPTOR-LIKE KINASE 1. IPK1 mutation did not prevent the induction of systemic acquired resistance by avirulent P. syringae. Also, ips2 and ips2/3 double mutant plants, like ipk1, were hyper-susceptible to Pseudomonas syringae but were not compromised in flg22-induced local acquired resistance. The results support the role of InsP6 biosynthesis enzymes in effective basal resistance and indicate that there is more than one basal resistance mechanism dependent upon InsP6 biosynthesis.