Analysis of long non-coding RNAs and mRNAs in harvested kiwifruit in response to the yeast antagonist, Wickerhamomyces anomalus

The diagrammatic model mechanisms involved in the disease resistance of kiwifruit induced by W. anomalous based on transcriptomic data obtained in the present study. The red font in the gray box indicates genes up-regulated by DE-lncRNA, which are distributed in different black virtual frames, and their functions are explained in the frame. It is speculated that DE-lncRNAs may be involved in regulating the up-regulated expression of these genes to improve the resistance of kiwifruit after W. anomalous stimulation. [Display omitted] •W. anomalus exhibits good biocontrol activity against blue and gray mold on kiwifruit.•LncRNAs in kiwifruit may be involved in activating plant hormone signal transduction pathways in response to the biocontrol yeast.•LncRNAs in kiwifruit may modulate the production of related TFs and secondary metabolites.•The expression of downstream defense-related genes in kiwifruit increases in response to the application of the biocontrol yeast. Biological control utilizing antagonistic yeasts is an effective method for controlling postharvest diseases. Long non-coding RNAs (lncRNAs) have been found to be involved in a variety of plant growth and development processes, including those associated with plant disease resistance. In the present study, the yeast antagonist, Wickerhamomyces anomalus, was found to strongly inhibit postharvest blue mold (Penicillium expansum) and gray mold (Botrytis cinerea) decay of kiwifruit. Additionally, lncRNA high-throughput sequencing and bioinformatic analysis was used to identify lncRNAs in W. anomalus-treated wounds in kiwifruit and predict their function based on putative target genes. Our results indicate that lncRNAs may be involved in increasing ethylene (ET), jasmonic acid (JA), abscisic acid (ABA), and auxin (IAA) levels, as well as activating signal transduction pathways that regulate the expression of several transcription factors (WRKY72, WRKY53, JUB1AP2). These transcription factors (TFs) then mediate the expression of downstream, defense-related genes (ZAR1, PAD4, CCR4, NPR4) and the synthesis of secondary metabolites, thus, potentially enhancing disease resistance. Notably, by stimulating the accumulation of antifungal compounds, such as phenols and lignin, disease resistance in kiwifruit was enhanced. Our study provides new information on the mechanism underlying the induction of disease resistance in kiwifruit by W. anomalus, as well as a new disease resistance strategy that can be used to