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AcPGIP 在猕猴桃(Actinidia chinensis)对灰葡萄孢菌响应中的作用。

The role of AcPGIP in the kiwifruit (Actinidia chinensis) response to Botrytis cinerea.

机构信息

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, China.

出版信息

Funct Plant Biol. 2021 Nov;48(12):1254-1263. doi: 10.1071/FP21054.

Abstract

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.

摘要

猕猴桃(Actinidia chinensis)富含营养和药用价值。然而,灰霉菌(Botrytis cinerea)是导致猕猴桃产业遭受巨大经济损失和食品安全问题的元凶。了解猕猴桃对灰霉菌采后响应的分子机制对于防止灰霉腐烂和增强抗性育种至关重要。本研究以猕猴桃品种‘红阳’为实验材料。克隆了 AcPGIP 基因,并通过病毒诱导的基因沉默(VIGS)技术探索 PGIP 基因在猕猴桃对 B. cinerea 抗性中的功能。AcPGIP 的病毒诱导沉默导致猕猴桃对 B. cinerea 的敏感性增强。分析了抗氧化酶、次生代谢物和内源激素,以研究猕猴桃对 B. cinerea 感染的反应。猕猴桃对 B. cinerea 感染有效激活了抗氧化酶和次生代谢产物的产生,与未感染果实相比,吲哚-3-乙酸(IAA)、赤霉素 3(GA3)和脱落酸(ABA)的含量显著增加。AcPGIP 的沉默使猕猴桃能够通过一种替代机制快速激活激素信号通路,从而触发对 B. cinerea 感染的防御反应。这些结果扩展了我们对猕猴桃抗病性调控机制的认识;进一步为猕猴桃抗病性的分子育种提供了基因资源储备。

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