Functional Characterization of PeMep Gene Reveals Its Roles in the Vegetative Growth, Stress Adaptation, and Virulence of Penicillium expansum

TL;DR

This study identifies a key gene in a fungus that causes apple decay, showing it's important for growth, stress resistance, and causing disease.

Contribution

The study reveals PeMep as a novel effector protein with roles in growth, stress adaptation, and virulence in Penicillium expansum.

Findings

PeMep deletion reduced fungal growth by 23% and conidiation by 23.3%.

The ΔPeMep mutant showed hypersensitivity to osmotic, oxidative, and thermal stresses.

Lesion sizes on apples were 15–30% smaller in the ΔPeMep mutant, indicating reduced virulence.

Abstract

Penicillium expansum, a major postharvest pathogen, causes blue mold decay in apples, resulting in substantial economic losses and mycotoxin contamination. Despite the importance of effector proteins in fungal pathogenicity, the role of metalloproteases in P. expansum remains unclear. Here, we characterize an effector candidate, PeMep, through whole genome sequencing and functional analyses. Functional validation confirmed the secretory capacity of its signal peptide via yeast assays and subcellular localization. Deletion of PeMep significantly impaired fungal growth (23% reduction), conidiation (23.3% decrease), and germination efficiency. The ΔPeMep mutant exhibited hypersensitivity to osmotic, oxidative, and thermal stresses, highlighting its vital role in environmental adaptability. Importantly, pathogenicity assays revealed attenuated virulence in the ΔPeMep mutant, with 15–30% smaller lesion sizes on apples and delayed hyphal penetration compared to the wild-type, demonstrating that PeMep is essential for the pathogenic process of P. expansum 3.3703. These findings identify PeMep as a potential multifunctional effector protein crucial for fungal development, environmental adaptation, and pathogenicity in P. expansum 3.3703, providing a novel target for postharvest disease management.

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