Loquat is a popular fruit widely cultivated all over the world. It is rich in minerals and carotenoids and has high commercial value. At room temperature, loquat fruit is impressionable to water and nutritional losses, physical damage, and microbial decay, resulting in a short postharvest life. Low-temperature storage is routinely used to prolong the shelf life of loquat fruit; however, cold storage can also lead to lignification of flesh tissue, which is one of the major symptoms of chilling injury (CI), reducing the quality and economic value of the fruit. In addition, fruit decay caused by microbial infection is another important reason for postharvest losses of loquat. To reduce quality deterioration and optimize the postharvest storage strategies of loquat fruit, considerable progress has been made in the physiological and molecular biological studies of CI, microbial decay, and preservation technologies of loquat fruit during the postharvest phase in recent decades. This review summarizes the current research progress and provides a reference for the improvement of loquat fruit quality.

The primary cause of postharvest loss in table grape fruit is attributed to gray mold, which is caused by Botrytis cinerea. The present study confirmed the inhibitory effects of nystatin on the growth and development of B. cinerea, which led to a remarkable reduction in the severity of gray mold on table grape fruits. Furthermore, the application of nystatin disrupted the membrane permeability of B. cinerea, causing increased cellular leakage and cell death. In addition, the transcriptome analysis showed that the application of nystatin effectively modulated the transcriptional profile of genes involved in ribosome and mitochondrion biogenesis, as well as oxidoreductase activity, thereby disrupting the homeostasis of cellular organelles. Moreover, the nystatin treatment down-regulated genes associated with membrane trafficking, protein degradation by the ubiquitin–proteasome system, and the autophagy process, ultimately attenuating the pathogenicity of B. cinerea. Collectively, nystatin can be considered a viable agent for managing gray mold on table grape fruit.

Anthracnose, caused by Colletotrichum gloeosporioides, is a destructive postharvest disease that substantially reduces the quality and shelf life of apple fruit. Effective and environmentally friendly strategies for controlling this disease remain limited. In this study, we investigated the antifungal activity of benzyl isothiocyanate (BITC), a naturally occurring sulfur-containing volatile organic compound, against C. gloeosporioides and explored its underlying mechanism of action. In vitro assays showed that BITC strongly inhibited fungal growth and development, with mycelial growth completely inhibited at 25 mg/L and spore germination as well as germ tube elongation completely suppressed at 30 mg/L. In vivo, BITC at 150 mg/L effectively suppressed anthracnose lesion expansion on apple fruit. Further mechanistic analyses demonstrated that BITC induced membrane lipid peroxidation, compromised membrane integrity, and caused the leakage of intracellular constituents, thereby markedly reducing spore viability. In addition, RT-qPCR analysis revealed that BITC significantly downregulated the expression of several key pathogenicity-related genes. Collectively, these findings indicate that BITC inhibits C. gloeosporioides by disrupting membrane integrity and suppressing pathogenicity, highlighting its potential as a natural antifungal agent for the management of postharvest apple anthracnose.