Wound‐response jasmonate dynamics in the primary vasculature

Abstract

Summary The links between wound‐response electrical signalling and the activation of jasmonate synthesis are unknown. We investigated damage‐response remodelling of jasmonate precursor pools in the Arabidopsis thaliana leaf vasculature. Galactolipids and jasmonate precursors in primary veins from undamaged and wounded plants were analysed using MS‐based metabolomics and NMR. In parallel, DAD1‐LIKE LIPASEs (DALLs), which control the levels of jasmonate precursors in veins, were identified. A novel galactolipid containing the jasmonate precursor 12‐oxo‐phytodienoic acid (OPDA) was identified in veins: sn‐2‐O‐(cis‐12‐oxo‐phytodienoyl)‐sn‐3‐O‐(β‐galactopyranosyl) glyceride (sn‐2‐OPDA‐MGMG). Lower levels of sn‐1‐OPDA‐MGMG were also detected. Vascular OPDA‐MGMGs, sn‐2‐18:3‐MGMG and free OPDA pools were reduced rapidly in response to damage‐activated electrical signals. Reduced function dall2 mutants failed to build resting vascular sn‐2‐OPDA‐MGMG and OPDA pools and, upon wounding, dall2 produced less jasmonoyl‐isoleucine (JA‐Ile) than the wild‐type. DALL3 acted to suppress excess JA‐Ile production after wounding, whereas dall2 dall3 double mutants strongly reduce jasmonate signalling in leaves distal to wounds. LOX6 and DALL2 function to produce OPDA and the non‐bilayer‐forming lipid sn‐2‐OPDA‐MGMG in the primary vasculature. Membrane depolarizations trigger rapid depletion of these molecules. We suggest that electrical signal‐dependent lipid phase changes help to initiate vascular jasmonate synthesis in wounded leaves.