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Unraveling bacterial glycosyrin as a master manipulator of plant glycobiology

Project description

Bacterial glycosyrin alters host carbohydrate metabolism to suppress immunity

Plants secrete an enzyme that strips protective sugars off bacterial flagella. Once this sugar ‘coating’ is removed, plant immune receptors can ‘see’ the bacteria and trigger an immune response. Recently, scientists discovered that the bacterial plant pathogen Pseudomonas syringae secretes the iminosugar molecule glycosyrin, which tricks the enzyme into binding it instead. With the support of the Marie Skłodowska-Curie Actions programme, the UNBAGMAP project seeks to demonstrate that glycosyrin acts as a versatile virulence factor, altering host carbohydrate metabolism to suppress plant defences. Integrating receptor biology, proteomics, metabolomics and functional infection assays, UNBAGMAP will shed light on bacterial metabolites in plant immune dysfunction with potential application to crop engineering.

Objective

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.

Fields of science (EuroSciVoc)

Keywords

Programme(s)

Topic(s)

Funding Scheme

HORIZON-TMA-MSCA-PF-EF - HORIZON TMA MSCA Postdoctoral Fellowships - European Fellowships

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Call for proposal

(opens in new window) HORIZON-MSCA-2025-PF

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Coordinator

THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF OXFORD
Net EU contribution
€ 260 347,92
Address
WELLINGTON SQUARE UNIVERSITY OFFICES
OX1 2JD Oxford
United Kingdom
Region
South East (England) Berkshire, Buckinghamshire and Oxfordshire Oxfordshire
Activity type
Higher or Secondary Education Establishments
Links
Total cost
No data