Our Work at UMAydis@IPMB

In a continuous arms race, U. maydis decorates its effector with glycans to target a host pectin methylesterase inhibitor (PMEI) that has evolved to escape fungal inhibition. By overriding this host evasion strategy, the fungus relieves PMEI-mediated inhibition, restoring plant PME activity and rendering demethylesterified pectins highly susceptible to host-derived pectinolytic enzymes to support virulence. 

bioRxiv, https://doi.org/10.1101/2025.04.01.646729

Maize AFP1 boosts fungal chitin levels by altering the activities of host cell-surface glycoproteins. This antifungal mechanism inhibits fungal cell development, blocks spore germination, and may prevent fungi from evading host recognition.

mBIO 2023. https://doi.org/10.1128/mbio.00093-23

This study reveals that U. maydis's cell-surface PR1-like protein uses dual activities to promote virulence. It senses plant phenolics to elicit hyphal-like growth while hijacking a maize protease to release CAPE-like peptides to subvert host defenses during infection. 

Nat. Commun. 2023. https://doi.org/10.1038/s41467-023-41459-4.