Functional analysis of AcARF18 in kiwifruit resistance to Botrytis cinerea.

BACKGROUND

Investigating the role of AcARF18 in resistance to Botrytis cinerea in kiwifruit (Actinidia chinensis) may enrich our understanding of the disease resistance regulatory mechanisms and provide genetic resource reserves for disease resistance molecular breeding in kiwifruit.

RESULTS

Virus-induced gene silencing was used to investigate the functional role of AcARF18 in kiwifruit against B. cinerea. Silencing of AcARF18 (AcARF18-TRV) enhanced the resistance of kiwifruit to B. cinerea, suggesting that AcARF18 might negatively regulate kiwifruit resistance to the fungal pathogen. Physiological index analysis showed that the activity of defense enzymes, and contents of total phenols and flavonoids, and the content of indole-3-acetic acid and salicylic acid were higher in AcARF18-TRV kiwifruit than that in the control group (CK) with or without B. cinerea. RNA-seq analysis with a log fold change of ≥1 and false discovery rate of <0.01 revealed 2184 differentially expressed genes (DEGs) in AcARF18-TRV versus CK comparison. Of these DEGs, 1130 were upregulated and 1054 were downregulated in the silenced group. The majority of the selected DEGs were enriched in 'secondary metabolite synthesis' and 'plant hormone signal transduction' pathways.

CONCLUSION

Our results reveal the molecular mechanism by which AcARF18 regulates kiwifruit resistance to B. cinerea, and further provide genetic resources for the molecular breeding of kiwifruit to enhance its disease resistance. © 2025 Society of Chemical Industry.