Poster
Liang Kong
University of Michigan
ANN ARBOR, Michigan, United States
Xiyu Ma
Texas A&M University
College Station, Texas, United States
Chao Zhang
University of Michigan
ANN ARBOR, Michigan, United States
Sung-Il Kim
University of Michigan
ANN ARBOR, Michigan, United States
Bo Li
Texas A&M University
College Station, Texas, United States
Yingpeng Xie
University of Michigan
ANN ARBOR, Michigan, United States
In-Cheol Yeo
University of Michigan
ANN ARBOR, Michigan, United States
Hem Thapa
Texas A&M University
College Station, Texas, United States
Sixue Chen
University of Mississippi
Oxford, Mississippi, United States
Timothy P. Devarenne
Texas A&M University
College Station, Texas, United States
Teun Munnik
University of Amsterdam
Amsterdam, Noord-Holland, Netherlands
Ping He
Professor
University of Michigan
Ann Arbor, MI, USA
Libo Shan
Professor
University of Michigan
Ann Arbor, MI, USA
Phosphatidic acid (PA) and reactive oxygen species (ROS) are rapidly induced upon immune activation to limit pathogen colonization. However, how PA is intertwined with ROS signaling remains unclear. Here, we report that Arabidopsis diacylglycerol kinase 5 (DGK5) is essential for PTI- and ETI-induced PA production. The pattern recognition receptor (PRR)-associated kinase BIK1 phosphorylates DGK5 at Ser-506, triggering a rapid PA burst and activating plant immunity. To avoid excessive PA accumulation, the PRR-activated intracellular kinase MPK4 phosphorylates DGK5 at Thr-446, suppressing its activity and maintaining PA homeostasis. Similarly, ETI activation induces DGK5 phosphorylation and DGK5-derived PA production. Notably, PA binds to and stabilizes the NADPH oxidase RBOHD, thereby regulating ROS production in plant PTI and ETI, and their potentiation. Our findings reveal that distinct phosphorylation of DGK5 by PRR-activated BIK1 and MPK4 fine-tunes cellular PA homeostasis that regulates ROS generation in coordinating two branches of plant immunity.