Alterations of flg22-signaling and innate immunity in loss of functional mutants of dynamin related protein network.    
G. EKANAYAKE (1) (1) Universiity of Missouri, U.S.A.

We utilize the FLS2- flagellin model system, in which the plant receptor Flagellin Sensing 2 (FLS2) perceives bacterial flagellin (or flg22) and induces immune responses. Ligand-induced endocytosis of FLS2 is important to desensitize cells to flg22 and remove activated FLS2 from the plasma membrane, likely to terminate signaling. In eukaryotes, dynamins and dynamin-related proteins (DRPs) are large GTPases that act as molecular scissors during clathrin-mediated endocytosis. Recently, we identified Arabidopsis DRP2B as a non-canonical regulator of flg22-signaling and immunity against Pseudomonas syringae. Loss of DRP2B also causes 20% decrease of flg22-induced endocytosis of FLS2. My goal is to identify proteins that function together with DRP2B in immunity and endocytosis of FLS2. In large-scale immunoprecipitation using an anti-DRP2B antibody, we identified several proteins including Vesicular Trafficking 3 (VES3). We have data showing that loss of VES3 resulted in similar flg22-defects as drp2b. Furthermore, ves3 null mutants were more susceptible to Pseudomonas syringae infection. I created a drp2b ves3 double mutant, which was seedling lethal confirming that DRP2B and VES3 function together in plant growth. Interestingly, drp2b/drp2b VES3/ves3 and DRP2B/drp2b ves3/ves3 mutant plants have growth defects, which were less severe than the double mutant. Currently, I am using these plants to test a potential synergistic role of VES3 and DRP2B in flg22-signaling and immunity.

Abstract Number: P18-666
Session Type: Poster