How Colletotrichum Effectors Shape Hemibiotrophic Infection: Implications for Postharvest Disease Control

Anthracnose diseases, caused by Colletotrichum spp., compromise both preharvest yield and postharvest quality of horticultural crops worldwide. Many Colletotrichum species infecting fruits and vegetables exhibit hemibiotrophic or functionally hemibiotrophic infection patterns: in numerous systems, infections initiated before harvest remain symptomless for a variable period and become aggressive as host ripening and senescence proceed. This switch is modulated by secreted effectors and virulence factors. Apoplastic effectors suppress extracellular pattern-triggered immunity (PTI), whereas cytoplasmic effectors target immune hubs, hormone signaling and chloroplast metabolism to prevent premature host cell death. At the transition, stage-specific enzymes and toxin-like proteins drive necrosis, tissue maceration, and decay. Although multi-omics has accelerated effector identification, functional redundancy and scarce in planta validation in natural horticultural hosts remain limiting. This review synthesizes how Colletotrichum effectors contribute to biotrophic compatibility, may participate in the biotrophy-to-necrotrophy transition, and support necrotrophic colonization. Because quiescent infections are initiated and conditioned in the field long before harvest, management of pre- and postharvest anthracnose must span the field-to-storage continuum—susceptibility-target breeding, preharvest diagnostics of quiescent infection, bio-inspired peptide and compound design, and targeted inhibition of virulence. We identify the conceptual and methodological bottlenecks that must be overcome.