Constitutive salicylic acid accumulation in pi4kIIIβ1β2 Arabidopsis plants stunts rosette but not root growth

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), pi4kIII beta 1 beta 2, 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 pi4kIII beta 1 beta 2 phenotype. The pi4kIII beta 1 beta 2 mutant accumulated a high concentration of salicylic acid (SA), constitutively expressed SA marker genes including PR-1, and was more resistant to Pseudomonas syringae. pi4kIII beta 1 beta 2 was crossed with SA signalling mutants eds1 and npr1 and SA biosynthesis mutant sid2 and NahG. The dwarf phenotype of pi4kIII beta 1 beta 2 rosettes was suppressed in all four triple mutants. Whereas eds1 pi4kIII beta 1 beta 2, sid2 pi4kIII beta 1 beta 2 and NahG pi4kIII beta 1 beta 2 had similar amounts of SA as the wild-type (WT), npr1pi4kIII beta 1 beta 2 had more SA than pi4kIII beta 1 beta 2 despite being less dwarfed. This indicates that PI4KIII beta 1 and PI4KIII beta 2 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 pi4kIII beta 1 beta 2 was not suppressed in any of the triple mutants. The pi4kIII beta 1 beta 2 mutations together cause constitutive activation of SA signalling that is responsible for the dwarf rosette phenotype but not for the short root phenotype.