文献类型：期刊文献

英文题名：Investigation of the role of AcTPR2 in kiwifruit and its response to Botrytis cinerea infection

作者：Li, Zhe-Xin[1] Lan, Jian-Bin[1] Liu, Yi-Qing[1] Qi, Li-Wang[2] Tang, Jian-Min[1]

第一作者：Li, Zhe-Xin

通信作者：Tang, JM[1];Qi, LW[2]

机构：[1]Chongqing Univ Arts & Sci, Inst Special Plants,Chongqing Key Lab Econ Plant, Coll Landscape Architecture & Life Sci, Collaborat Innovat Ctr Special Plant Ind Chongqin, Yongchuan 402160, Peoples R China;[2]Chinese Acad Forestry, Res Inst Forestry, State Key Lab Tree Genet & Breeding, Beijing 100091, Peoples R China

年份：2020

卷号：20

期号：1

外文期刊名：BMC PLANT BIOLOGY

收录：;Scopus(收录号：2-s2.0-85097432342);WOS:【SCI-EXPANDED(收录号:WOS:000599856800004)】；

基金：The authors are grateful for the financial support provided by National Natural Science Foundation of China (32001351 and 31670688) to conduct research design and most of the experiment, Natural Science Foundation of Chongqing (cstc2018jscx-msybX0196) in data analysis and manuscript writing, and to cultivate materials used in the present study.

语种：英文

外文关键词：AcTPR2; Botrytis cinerea; IAA signaling; Kiwifruit; Virus-induced gene silencing

摘要：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 (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.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.