The role of Ca2+ signalling in OG-triggered immunity

Cell wall damage, provoked by injury or pathogens, releases various Damage-Associated Molecular Patterns (DAMPs) that are recognized by pattern recognition receptors (PRRs), triggering defense responses. Oligogalacturonides (OGs) are typical cell wall-derived DAMPs, whose accumulation is facilitated when microbial polygalacturonases (PGs) interact with plant inhibitors (PGIPs). OGs perception induces Pattern Triggered Immunity (PTI)-like responses, including a Ca2+-mediated signal. A PGIP-PG chimera, named OG-machine (OGM), expressed in Arabidopsis plants under an inducible promoter, release OGs in vivo, conferring resistance to pathogens but posing the risk of a detrimental hyper-immunity due to excessive OGs accumulation. A homeostatic control mechanism mediated by specific OG oxidases (OGOXs) belonging to the Berberine Bridge Enzyme-like (BBE-like) protein family exists to mitigate the adverse impact of OG action. Activation of defense responses, such as up-regulation of defense genes, is reduced in plants overexpressing OGOX enzymes but increased in ogox knockout mutants. Employing Arabidopsis plants expressing different calcium biosensors (GCaMP3 and YC3.6-NES) in backgrounds altered in OGOX expression and in the OGM background, we aim to investigate how variations in Ca2+ signalling underlie the altered elicitor activity of OGs and elucidate the cytosolic [Ca2+] dynamics in hyper-immunity due to excessive OG accumulation.