Quiescence of postharvest pathogens: a fungal inhibition process or an immune response of the unripe host fruit?

Postharvest pathogens can infect fresh produce both before and after harvest, by direct or wound-enhanced penetration, remaining quiescent until ripening. Biotrophic-like postharvest pathogens persist beneath host cells and can remain in a state of quiescence. They detect environmental cues and regulate quiescence through chromatin-level control and the secretion of effectors that interact with host pattern recognition receptors. By contrast, necrotrophic fungi persist between dead cells and depend more directly on nutrient availability to prime their growth and upon secretion for fungal virulence factors. During quiescence, the host also mounts specific responses, including activation of pattern recognition receptor genes, ethylene signaling (particularly in unripe fruit), and defense genes such as PR-10 and chitinases. Jasmonic acid and ethylene pathways synergistically enhance these defenses. As fruit ripens, the transition from quiescence to active necrotrophic growth is triggered, accelerating tissue decay. This activation is driven by several key factors, including weakened host defenses, decreased levels of antifungal compounds such as polyphenols, increased cell wall accessibility due to fruit softening and ripening-associated changes in signaling pathways, which alter environmental pH, carbon metabolism, and secondary metabolite production. These regulatory mechanisms collectively govern the timing and extent of fungal initiation of colonization during fruit senescence.