Chongqing Key Laboratory of Economic Plant Biotechnology, Collaborative Innovation Center of Special Plant Industry in Chongqing, College of Landscape Architecture and Life Science/ Institute of Special Plants, Chongqing University of Arts and Sciences, Yongchuan, 402160, P.R. China.
State Key Laboratory of Tree Genetics and Breeding, Research Institute of Forestry, Chinese Academy of Forestry, Beijing, 100091, P.R. China.
BMC Plant Biol. 2020 Dec 10;20(1):557. doi: 10.1186/s12870-020-02773-x.
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.
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), 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.
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.
阐明猕猴桃对灰霉病的反应调控机制可为其分子育种提供基础，以赋予其对该疾病的抗性。在这项研究中，以‘红阳’猕猴桃为实验材料；克隆出 TOPLESS/TOPLESS-RELATED (TPL/TPR) 共抑制子基因 AcTPR2 到 pTRV2 载体（AcTPR2-TRV）中，并利用病毒诱导的基因沉默技术来建立 AcTPR2 基因在猕猴桃对灰霉病抗性中的功能。
AcTPR2 的病毒诱导沉默增强了猕猴桃对灰霉病的易感性。检测到防御酶如超氧化物歧化酶（SOD）、过氧化物酶（POD）、过氧化氢酶（CAT）和苯丙氨酸解氨酶（PAL）以及内源性植物激素如吲哚乙酸（IAA）、赤霉素（GA）、脱落酸（ABA）和水杨酸（SA）。猕猴桃激活这些酶和内源性植物激素以应对病原体诱导的应激和损伤。IAA 信号基因-AcNIT、AcARF1 和 AcARF2 的表达水平在 AcTPR2-TRV 处理组中高于对照组。AcTPR2-TRV 猕猴桃中的 IAA 水平较高，腐烂表型比对照组更严重。这些结果表明，AcTPR2 的下调促进了 IAA 和 IAA 信号基因的表达，并加速了采后猕猴桃的衰老。此外，灰霉病显著上调了 AcTPR2，表明 AcTPR2 通过下调 IAA 和 IAA 信号基因增强了猕猴桃对病原体的防御。
本研究的结果有助于阐明猕猴桃抗病性的调控机制，并为猕猴桃抗病性的分子育种提供遗传资源。
