Revisiting the current and emerging concepts of postharvest fresh fruit and vegetable pathology for next-generation antifungal technologies.

Fungal infections of fresh fruits and vegetables (FFVs) can lead to safety problems, including consumer poisoning by mycotoxins. Various strategies exist to control fungal infections of FFVs, but their effectiveness and sustainability are limited. Recently, new concepts based on the microbiome and pathobiome have emerged and offer a more holistic perspective for advancing postharvest pathogen control techniques. Understanding the role of the microbiome in FFV infections is essential for developing sustainable control strategies. This review examines current and emerging approaches to postharvest pathology. It reviews what is known about the initiation and development of infections in FFVs. As a promising concept, the pathobiome offers new insights into the basic mechanisms of microbial infections in FFVs. The underlying mechanisms uncovered by the pathobiome are being used to develop more relevant global antifungal strategies. This review will also focus on new technologies developed to target the microbiome and members of the pathobiome to control infections in FFVs and improve safety by limiting mycotoxin contamination. Specifically, this review stresses emerging technologies related to FFVs that are relevant for modifying the interaction between FFVs and the microbiome and include the use of microbial consortia, the use of genomic technology to manipulate host and microbial community genes, and the use of databases, deep learning, and artificial intelligence to identify pathobiome markers. Other approaches include programming the behavior of FFVs using synthetic biology, modifying the microbiome using sRNA technology, phages, quorum sensing, and quorum quenching strategies. Rapid adoption and commercialization of these technologies are recommended to further improve the overall safety of FFVs.

Infection of postharvest pear by Penicillium expansum is facilitated by the glycoside hydrolase (eglB) gene.

The primary reason for postharvest loss is blue mold disease which is mainly caused by Penicillium expansum. Strategies for disease control greatly depend on the understanding of mechanisms of pathogen-fruit interaction. A member of the glycoside hydrolase family, ß-glucosidase 1b (eglB), in P. expansum was significantly upregulated during postharvest pear infection. Glycoside hydrolases are a large group of enzymes that can degrade plant cell wall polymers. High homology was found between the glycoside hydrolase superfamily in P. expansum. Functional characterization and analysis of eglB were performed via gene knockout and complementation analysis. Although eglB deletion had no notable effect on P. expansum colony shape or microscopic morphology, it did reduce the production of fungal hyphae, thereby reducing P. expansum's sporulation and patulin (PAT) accumulation. Moreover, the deletion of eglB (ΔeglB) reduced P. expansum pathogenicity in pears. The growth, conidia production, PAT accumulation, and pathogenicity abilities of ΔeglB were restored to that of wild-type P. expansum by complementation of eglB (ΔeglB-C). These findings indicate that eglB contributes to P. expansum's development and pathogenicity. This research is a contribution to the identification of key effectors of fungal pathogenicity for use as targets in fruit safety strategies.

The necrosis-inducing protein (NIP) gene contributes to Penicillium expansum virulence during postharvest pear infection.

Penicillium expansum is the causative fungus of blue mold decay in postharvest pears resulting in substantial economic losses. Investigating P. expansum-pear fruit interactions is necessary to help develop P. expansum control strategies for effective and safe pear production. Investigating the P. expansum gene expression alterations and essential gene functions during the infection process is indispensable. Based on our results, the necrosis-inducing protein (NIP) gene was closely associated with genes related to plant cell wall degrading enzymes (CWDEs) and involved in P. expansum virulence. The NIP has high homology with other already-known fungal NIPs. To evidence the role of NIP in P. expansum virulence, NIP mutant (including knockout (ΔNIP) and complementation mutant (cNIP)) P. expansum were generated. Despite the NIP deletion did not affect the basic morphology and structure of P. expansum, it slowed down the fungal growth and hyphal production, thus reducing P. expansum's sporulation and patulin (PAT) accumulation. Furthermore, the deletion of NIP reduced the pathogenicity of P. expansum in pear. The complementation of NIP (cNIP) restored the growth, conidia production, PAT accumulation, and virulence of ΔNIP to the level of wild-type P. expansum. In addition, PAT can cause decay and aggravate the disease severity of wild-type P. expansum and ΔNIP on pears. Our results confirmed NIP plays a crucial role in P. expansum's growth, hyphal production, and pathogenicity in pears.

Transcriptome Characterization and Expression Profiles of Disease Defense-Related Genes of Table Grapes in Response to Pichia anomala Induced with Chitosan.

Transcriptome analysis (TA) was conducted to characterize the transcriptome changes in postharvest disease-related genes of table grapes following treatment with Pichia anomala induced with chitosan (1% w/v). In the current study, the difference in the gene expression of table grapes after treatment with P. anomala induced with chitosan and that of a control group was compared 72 h post-inoculation. The study revealed that postharvest treatment of table grapes with P. anomala induced with chitosan could up-regulate genes that have a pivotal role in the fruit's disease defense. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) results also confirmed that GO terms and the KEGG pathways, which have pivotal roles in plant disease resistance, were significantly enriched. The up-regulated genes of the treatment group have a unique function in the fruit's disease resistance compared to the control group. Generally, most genes in the plant-pathogen interaction pathway; the plant Mitogen-activated protein kinase (MAPK) signaling pathway; the plant hormone signal transduction pathway; the pathway of glutathione metabolism; the pathway of phenylalanine, tyrosine, and tryptophan biosynthesis; and the pathway of flavonoid biosynthesis were all up-regulated. These up-regulations help the fruit to synthesize disease-resistant substances, regulate the reactive oxygen species (ROS), enhance the fruit cell wall, and enrich hormone signal transduction during the pathogen's attack. This study is useful to overcome the lags in applying transcriptomics technology in postharvest pathology, and will provide insight towards developing other alternative methods to using bio-pesticides to control postharvest diseases of perishables.