Unraveling bacterial glycosyrin as a master manipulator of plant glycobiology

The apoplast is a critical battlefield where host immunity and microbial virulence collide. Plants rely on pattern recognition receptors (PRRs) and defense metabolites to sense and restrict microbial invasion, while pathogens evolve countermeasures to subvert these processes. Recent studies revealed that Pseudomonas syringae secretes glycosyrin, a unique iminosugar that promotes virulence by targeting the plant-secreted β-galactosidase BGAL1. BGAL1 is required for releasing the immunogenic flg22 epitope from glycosylated flagella, and glycosyrin blocks this process by inhibiting BGAL1. Beyond this specific role, emerging evidence implys that glycosyrin can broadly interfere with host glycobiology, potentially disrupting immune receptor maturation, blocking defense hormone release, and directly enhancing pathogen fitness.This project aims to establish glycosyrin as a multi-faceted virulence factor that reprogrammes plant glycobiology to undermine immunity. Three objectives will be pursued: (1) reveal how glycosyrin deregulates immune receptor function through altered glycosylation and reduced receptor accumulation; (2) demonstrate how glycosyrin suppresses the release of salicylic acid from inactive conjugates, thereby dampening systemic immunity; and (3) determine how glycosyrin promotes osmoprotection by inducing the accumulation of apoplastic osmolytes that enhance pathogen survival under stress. These objectives will be addressed through a multidisciplinary strategy integrating receptor biology, proteomics, metabolomics, and functional infection assays. By revealing glycosyrin as a molecular weapon that hijacks glycosidase-dependent processes, this work will redefine how bacterial metabolites can manipulate host immunity. The results will deliver a step-change in our understanding of plant–pathogen interactions at the interface of glycobiology and immunity, while opening new avenues for engineering durable resistance in crops.