Abstract
BackgroundElucidation 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.ResultsVirus-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 (GA3), 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.ConclusionsThe 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.
Highlights
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
PCR detection of resistant colonies bearing the AcTPR2-TRV2 construct was performed to confirm that the silencing fragment was successfully ligated onto the pTRV2 vector (Fig. 1c)
AcTPR2 expression was greatly reduced in AcTPR2-TRV fruits Agrobacterium GV3101 harboring the AcTPR2-TRV2 expression vector (AcTPR2-TRV), sterilized ddH2O (WT), and the vector pTRV1–2 (TRV), were transformed to ‘Hongyang’ kiwifruit by transient injection
Summary
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. Kiwifruit (Actinidia chinensis L.) is prone to fungal pathogen infections that cause major postharvest crop losses and may render the fruit unsafe for consumers. Botrytis cinerea (B. cinerea) is a fungal pathogen responsible for gray mold. It can damage or destroy ≤30% of the kiwifruit crop [1]. In order to breed gray mold resistance into kiwifruit, it is first necessary to elucidate the mechanism regulating plant pathogen response. Current research on gray mold control has focused mainly on physical, chemical, and certain biological controls [2,3,4,5]. The regulatory and signaling pathways associated with the genes controlling disease resistance in kiwifruit remain to be determined
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