Lipid phosphorylation by a diacylglycerol kinase suppresses ABA biosynthesis to regulate plant stress responses.

Abstract

Lipid phosphorylation by diacylglycerol kinase (DGK) that produces phosphatidic acid (PA) plays important roles in various biological processes, including stress responses, but the underlying mechanisms remain elusive. Here, we show that DGK5 and its lipid product PA suppress ABA biosynthesis by interacting with ABA-DEFICIENT 2 (ABA2), a key ABA biosynthesis enzyme, to negatively modulate plant response to abiotic stress tested in Arabidopsis thaliana. Loss of DGK5 function rendered plants less damaged, whereas overexpression (OE) of DGK5 enhanced plant damage to water and salt stress. The dgk5 mutant plants exhibited decreased total cellular and nuclear levels of PA with increased levels of diacylglycerol, whereas DGK5-OE plants displayed the opposite effect. Interestingly, we found that both DGK5 and PA bind to the ABA-synthesizing enzyme ABA2 and suppress its enzymatic activity. Consistently, the dgk5 mutant plants exhibited increased levels of ABA, while DGK5-OE plants showed reduced ABA levels. In addition, we showed that both DGK5 and ABA2 are detected in and outside the nuclei, and loss of DGK5 function decreased the nuclear association of ABA2. We found that both DGK5 activity and PA promote nuclear association of ABA2. Taken together, these results indicate that both DGK5 and PA interact with ABA2 to inhibit its enzymatic activity and promote its nuclear sequestration, thereby suppressing ABA production in response to abiotic stress. Our study reveals a sophisticated mechanism by which DGK5 and PA regulate plant stress responses.