The inhibition of basal phosphoinositide-dependent phospholipase C activity in Arabidopsis suspension cells by abscisic or salicylic acid acts as a signalling hub accounting for an important overlap in transcriptome remodelling induced by these hormones

• ABA and SA inhibit basal PI-PLC in Arabidopsis suspension cells.
• ABA, contrary to SA, does not lead to increase in phosphoinositides.
• We detect a major overlap between the transcriptomic responses to ABA and to SA.
• The overlap concerns genes that respond similarly to inhibitors of the PI-PLC pathway.
• Our analysis suggests a central role of this enzyme in hormonal cross-talk.

We show that both abscisic acid (ABA) and salicylic acid (SA) inhibit in vivo basal PI-PLC activity in Arabidopsis suspension cells. However, SA also activates in vivo phosphatidylinositol phosphorylation, which ABA does not. The transcriptome response of Arabidopsis suspension cells to a 4 h ABA treatment was compared to that of cells treated with U73122 or wortmannin, inhibitors of phospholipase C (PLC) and of the phosphatidylinositol-4-kinase that provides substrates to PLC, respectively. A clear over representation of genes for which ABA and these inhibitors have similar effects can be observed. Furthermore, 28% of ABA-induced genes were also induced by SA, while 40% of ABA-repressed genes were also repressed by SA. A similarity search in publically accessible transcriptome data confirms that those genes are also similarly regulated in response to ABA and SA in seedlings. We have shown that some of the SA responsive genes responded via an increase in phosphorylated phosphatidylinositol (phosphoinositides), while others did so via the activation of a phospholipase D pathway, and that the SA response of other genes was mimicked by the inhibition of PI-PLC. Interestingly, the pool of genes similarly regulated by SA and ABA is impoverished in genes responsive to SA via phosphoinositides but is enriched in those for which the response to SA is mimicked by the inhibition of PI-PLC. The increase in phosphoinositide appears to be an important process explaining the SA-specific response, while inhibition of a basal PI-PLC might contribute to the common ABA and SA transcriptomic responses.