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Background  Elucidation of the regulatory mechanism of kiwifruit response to gray mold disease caused by  Botrytis cinerea  can provide the basis for its molecular breeding to impart resistance against this disease. In this study, ‘Hongyang’ kiwifruit served as the experimental material; the TOPLESS/TOPLESS-RELATED (TPL/TPR) co-repressor gene  AcTPR2  was cloned into a pTRV2 vector ( AcTPR2 -TRV) and the virus-induced gene silencing technique was used to establish the functions of the  AcTPR2  gene in kiwifruit resistance to  Botrytis cinerea .    Results  Virus-induced silencing of  AcTPR2  enhanced the susceptibility of kiwifruit to  Botrytis cinerea . Defensive enzymes such as superoxide dismutase (SOD), peroxidase (POD), catalase (CAT), and phenylalanine ammonia-lyase (PAL) and endogenous phytohormones such as indole acetic acid (IAA), gibberellin (GA 3 ), abscisic acid (ABA), and salicylic acid (SA) were detected. Kiwifruit activated these enzymes and endogenous phytohormones in response to pathogen-induced stress and injury. The expression levels of the IAA signaling genes— AcNIT ,  AcARF1 , and  AcARF2 —were higher in the  AcTPR2 -TRV treatment group than in the control. The IAA levels were higher and the rot phenotype was more severe in  AcTPR2 -TRV kiwifruits than that in the control. These results suggested that  AcTPR2  downregulation promotes expression of IAA and IAA signaling genes and accelerates postharvest kiwifruit senescence. Further,  Botrytis cinerea  dramatically upregulated  AcTPR2,  indicating that  AcTPR2  augments kiwifruit defense against pathogens by downregulating the IAA and IAA signaling genes.    Conclusions  The results of the present study could help clarify the regulatory mechanisms of disease resistance in kiwifruit and furnish genetic resources for molecular breeding of kiwifruit disease resistance.    Supplementary Information  The online version contains supplementary material available at 10.1186/s12870-020-02773-x.

Investigation of the role of AcTPR2 in kiwifruit and its response to Botrytis cinerea infection