Tissue injury leads to the production of powerful lipid-based signaling molecules in both animals and plants. In flowering plants like Arabidopsis thaliana, plastidial membranes are the source of oxygenated lipids that eventually result in Jasmoni Acid (JA) biosynthesis. The JA phytohormone pathway is essential for plant defense against various stresses, including insect attacks, pathogenic infections, physical injury, and drought. In fact, insect herbivory alone is responsible for over 20% of global crop losses, and plants that cannot activate JA signaling are highly vulnerable to chewing insects. Although the JA pathway has been well-characterized at the molecular level, it remains unclear how are damage signals transmitted to plastids to initiate hormone production, and what is the nature of these signals. Our previous research revealed that changes in turgor pressure caused by osmotic stress can also trigger JA biosynthesis. This led us to propose a new hypothesis: mechanical signals may travel through plant tissues and cells, altering plastidilial membrane properties in a way that enables JA biosynthesis enzymes to access their substrates. To investigate this, we are quantifying the mechanical forces and osmotic pressures needed to induce JA production. We are also studying how these stress signals are transmitted to plastids, how changes in plastid membrane properties affect JA precursor synthesis, and which genetic components are involved in sensing and interpreting these biophysical cues. By uncovering the cellular, biophysical, and genetic mechanisms that initiate JA biosynthesis, we aim to deepen our understanding of how plants perceive and respond to environmental stress, ultimately contributing to strategies that enhance plant resilience.
