Descripción del proyecto
Both animals and plants produce potently active mediators in response to tissue injury. These oxygenated lipid derivatives include leukotrienes and prostaglandins in animals, and jasmonates (JAs) in plants with JA-Ile serving as the bioactive phytohormone in angiosperms. JAs are synthesized from poly unsaturated fatty acids residing in plant-specific plastidial membranes, and are essential to protect plants against numerous biotic and abiotic challenges including insect herbivory and temperature extremes. Despite the vital roles of JAs in sustaining plant fitness and although JA-Ile biosynthesis and signalling are well characterized, it is still unknown how are damage signals transmitted to plastids to initiate phytohormone production and what is the nature of the transmitted signal(s). Our previous work in Arabidopsis uncovered that osmotically-induced turgor pressure changes elicit JA-Ile biosynthesis. We hence hypothesise that JA-Ile biosynthesis initiation may result from the transmission of mechanical signals through tissues and cell compartments leading to biophysical changes of plastidial membranes granting substrate accessibility to JA biosynthesis enzymes. To address these central questions in plant biology we aim to:
1. Quantify the mechanical forces and osmotic pressure changes required to induce JA biosynthesis
2. Characterize cellular events that transduce mechanical and osmotic stress signals to plastids for JA-Ile precursor production
3. Alter plastidial biophysical parameters and study the consequences on JA-Ile precursor production
4. Identify genetic components involved in sensing and decoding biophysical stimuli for JA-Ile production
This proposal thus intends to fill a critical gap in knowledge on stress phytohormone biology regulating plant acclimation and, concomitantly, expand our understanding on fundamental aspects of plant mechano- and osmo-sensing.