The role of

Kiwifruit (Actinidia chinensis) is rich in nutritional and medicinal value. However, the organism responsible for grey mould, Botrytis cinerea, causes great economic losses and food safety problems to the kiwifruit industry. Understanding the molecular mechanism underlying postharvest kiwifruit responses to B. cinerea is important for preventing grey mould decay and enhancing resistance breeding. Kiwifruit cv. ‘Hongyang’ was used as experimental material. The AcPGIP gene was cloned and virus-induced gene silencing (VIGS) was used to explore the function of the polygalacturonase inhibiting protein (PGIP) gene in kiwifruit resistance to B. cinerea. Virus-induced silencing of AcPGIP resulted in enhanced susceptibility of kiwifruit to B. cinerea. Antioxidant enzymes, secondary metabolites and endogenous hormones were analysed to investigate kiwifruit responses to B. cinerea infection. Kiwifruit effectively activated antioxidant enzymes and secondary metabolite production in response to B. cinerea, which significantly increased Indole-3-acetic acid (IAA), gibberellin 3 (GA3) and abscisic acid (ABA) content relative to those in uninfected fruit. Silencing of AcPGIP enabled kiwifruit to quickly activate hormone-signaling pathways through an alternative mechanism to trigger defence responses against B. cinerea infection. These results expand our understanding of the regulatory mechanism for disease resistance in kiwifruit; further, they provide gene-resource reserves for molecular breeding of kiwifruit for disease resistance.