ABSTRACT
Phospholipids have recently been found to be integral elements of hormone signalling pathways. An Arabidopsis thaliana double mutant in two type III phosphatidylinositol-4-kinases (PI4Ks), pi4kIIIß1ß2, displays a stunted rosette growth. The causal link between PI4K activity and growth is unknown. Using microarray analysis, quantitative reverse transcription polymerase chain reaction (RT-qPCR) and multiple phytohormone analysis by LC-MS we investigated the mechanism responsible for the pi4kIIIß1ß2 phenotype. The pi4kIIIß1ß2 mutant accumulated a high concentration of salicylic acid (SA), constitutively expressed SA marker genes including PR-1, and was more resistant to Pseudomonas syringae. pi4kIIIß1ß2 was crossed with SA signalling mutants eds1 and npr1 and SA biosynthesis mutant sid2 and NahG. The dwarf phenotype of pi4kIIIß1ß2 rosettes was suppressed in all four triple mutants. Whereas eds1 pi4kIIIß1ß2, sid2 pi4kIIIß1ß2 and NahG pi4kIIIß1ß2 had similar amounts of SA as the wild-type (WT), npr1pi4kIIIß1ß2 had more SA than pi4kIIIß1ß2 despite being less dwarfed. This indicates that PI4KIIIß1 and PI4KIIIß2 are genetically upstream of EDS1 and need functional SA biosynthesis and perception through NPR1 to express the dwarf phenotype. The slow root growth phenotype of pi4kIIIß1ß2 was not suppressed in any of the triple mutants. The pi4kIIIß1ß2 mutations together cause constitutive activation of SA signalling that is responsible for the dwarf rosette phenotype but not for the short root phenotype.
