Emerging studies have suggested that there is a close link between inositol phosphate (InsP) metabolism and cellular phosphate (P_i ) homeostasis in eukaryotes; however, whether a common InsP species is deployed as an evolutionarily conserved metabolic messenger to mediate P_i signaling remains unknown. Here, using genetics and InsP profiling combined with P_i -starvation response (PSR) analysis in Arabidopsis thaliana, we showed that the kinase activity of inositol pentakisphosphate 2-kinase (IPK1), an enzyme required for phytate (inositol hexakisphosphate; InsP₆ ) synthesis, is indispensable for maintaining P_i homeostasis under P_i -replete conditions, and inositol 1,3,4-trisphosphate 5/6-kinase 1 (ITPK1) plays an equivalent role. Although both ipk1-1 and itpk1 mutants exhibited decreased levels of InsP₆ and diphosphoinositol pentakisphosphate (PP-InsP₅ ; InsP₇ ), disruption of another ITPK family enzyme, ITPK4, which correspondingly caused depletion of InsP₆ and InsP₇ , did not display similar P_i -related phenotypes, which precludes these InsP species from being effectors. Notably, the level of d/l-Ins(3,4,5,6)P₄ was concurrently elevated in both ipk1-1 and itpk1 mutants, which showed a specific correlation with the misregulated P_i phenotypes. However, the level of d/l-Ins(3,4,5,6)P₄ is not responsive to P_i starvation that instead manifests a shoot-specific increase in the InsP₇ level. This study demonstrates a more nuanced picture of the intersection of InsP metabolism and P_i homeostasis and PSRs than has previously been elaborated, and additionally establishes intermediate steps to phytate biosynthesis in plant vegetative tissues.

Wei‐Chi Lin

Publications