Actin dynamics contribute to the innate immune response of Arabidopsis
C. STAIGER (1), J. Li (2), J. Henty-Ridilla (2), L. Cao (2), J. Chang (3), B. Day (4) (1) Purdue University, U.S.A.; (2) Purdue University, U.S.A.; (3) Oregon State University, U.S.A.; (4) Michigan State University, U.S.A.

Recognition of MAMPs by pattern recognition receptors (PRRs) initiates rapid and long-term signaling events that contribute to defense against microbial invaders. Whether these events elicit cytoskeletal rearrangement and by what molecular mechanisms remains obscure. Using live-cell imaging, we characterized actin remodeling that occurs during pattern-triggered immunity (PTI) in Arabidopsis. We find that epidermal cells respond to various MAMPs by transiently increasing actin filament dynamics and elevating the density of filament arrays and that actin remodeling requires perception of MAMPs by cognate PRRs. To elucidate which actin-binding proteins are involved, we screened a collection of mutants expressing a cytoskeletal reporter. Actin-depolymerizing factor (ADF) and capping protein (CP) are implicated in transducing early signaling events into actin remodeling. The cp mutants fail to respond to MAMPs and are more susceptible than wild-type to Pseudomonas syringae DC3000. Because phospholipase D (PLD) activity and phosphatidic acid (PA) are implicated in PTI, and CP is a PA-binding protein, we tested whether actin remodeling depends on phospholipid fluxes. Exogenous PA treatment mimics the increase in actin density observed during PTI, whereas chemical inhibitors of PLD abrogate the cytoskeletal response to MAMPs. We propose a model whereby PRR activation results in PLD/PA signaling that inhibits CP leading to increased actin polymerization during innate immunity.

Abstract Number: C11-2, P7-223
Session Type: Concurrent