A fungal extracellular effector inactivates plant polygalacturonase-inhibiting protein.
Wei WeiLiangsheng XuHao PengWenjun ZhuKiwamu TanakaJiasen ChengKaren A SanguinetGeorge VandemarkWeidong ChenPublished in: Nature communications (2022)
Plant pathogens degrade cell wall through secreted polygalacturonases (PGs) during infection. Plants counteract the PGs by producing PG-inhibiting proteins (PGIPs) for protection, reversibly binding fungal PGs, and mitigating their hydrolytic activities. To date, how fungal pathogens specifically overcome PGIP inhibition is unknown. Here, we report an effector, Sclerotinia sclerotiorum PGIP-INactivating Effector 1 (SsPINE1), which directly interacts with and functionally inactivates PGIP. S. sclerotiorum is a necrotrophic fungus that causes stem rot diseases on more than 600 plant species with tissue maceration being the most prominent symptom. SsPINE1 enhances S. sclerotiorum necrotrophic virulence by specifically interacting with host PGIPs to negate their polygalacturonase-inhibiting function via enhanced dissociation of PGIPs from PGs. Targeted deletion of SsPINE1 reduces the fungal virulence. Ectopic expression of SsPINE1 in plant reduces its resistance against S. sclerotiorum. Functional and genomic analyses reveal a conserved virulence mechanism of cognate PINE1 proteins in broad host range necrotrophic fungal pathogens.
Keyphrases
- cell wall
- antimicrobial resistance
- escherichia coli
- pseudomonas aeruginosa
- staphylococcus aureus
- regulatory t cells
- signaling pathway
- biofilm formation
- dendritic cells
- gram negative
- binding protein
- type iii
- poor prognosis
- transcription factor
- multidrug resistant
- genome wide
- cancer therapy
- single cell
- immune response
- amino acid
- small molecule
- heat stress
- protein kinase