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采后番茄释放的乙烯和苯甲醛通过与 G 蛋白偶联受体结合并通过 cAMP 信号通路传递来抑制真菌。

Ethylene and Benzaldehyde Emitted from Postharvest Tomatoes Inhibit via Binding to G-Protein Coupled Receptors and Transmitting with cAMP-Signal Pathway of the Fungus.

机构信息

State Key Laboratory of Ecological Pest Control for Fujian and Taiwan Crops & College of Horticulture , Fujian Agriculture and Forestry University Fujian , 350013 Fuzhou , Fujian , P. R. China.

Institute of Plant Protection , Fujian Academy of Agricultural Sciences , 350013 Fuzhou , Fujian , P. R. China.

出版信息

J Agric Food Chem. 2019 Dec 11;67(49):13706-13717. doi: 10.1021/acs.jafc.9b05778. Epub 2019 Nov 25.

DOI:10.1021/acs.jafc.9b05778
PMID:31693347
Abstract

Tomato storage conditions are difficult largely due to infection which causes gray mold disease. However, the effects of the volatile organic compounds (VOCs) emitted by postharvest tomatoes on this fungus remain unclear. We analyzed the effects of tomato-emitted VOCs on pathogenicity, germination, and hyphal growth with bioassay, predicted the causative active compounds by principle component analysis, identified G-protein-coupled receptors (GPCRs) which captured chemical signals in the genome by stimulating molecular docking, tested the binding affinities of these receptors for the active compounds by fluorescence binding competition assay, and identified an associated signaling pathway by RNA interfere. The VOCs emitted by postharvest tomatoes inhibited ; ethylene and benzaldehyde were the active compounds causing this effect. One of the identified GPCRs in , BcGPR3, bound tightly to both active compounds. Two genes associated with the cAMP signaling pathway ( and ) were downregulated in wild-type exposed to the active compounds, as well as in the Δ mutant. Exposure to postharvest tomato VOCs reduces pathogenicity due to ethylene and benzaldehyde volatiles. The BcGPR3 protein is inactivated by the active compounds, and thus fails to transmit signals to the cAMP pathway, thereby inhibiting .

摘要

番茄贮藏条件困难,主要是由于感染导致灰霉病。然而,采后番茄释放的挥发性有机化合物(VOCs)对这种真菌的影响尚不清楚。我们通过生物测定分析了番茄释放的 VOCs 对病原菌致病性、萌发和菌丝生长的影响,通过主成分分析预测了致病活性化合物,通过刺激分子对接在基因组中鉴定了捕获化学信号的 G 蛋白偶联受体(GPCR),通过荧光结合竞争测定测试了这些受体与活性化合物的结合亲和力,并通过 RNA 干扰鉴定了相关信号通路。采后番茄释放的 VOCs 抑制了病菌的生长;乙烯和苯甲醛是导致这种效应的活性化合物。在 中鉴定的一个 GPCR,BcGPR3,与这两种活性化合物紧密结合。在暴露于活性化合物的野生型 中,与 cAMP 信号通路相关的两个基因(和)下调,在 Δ 突变体中也是如此。由于乙烯和苯甲醛挥发物,采后番茄 VOCs 降低了病菌的致病性。BcGPR3 蛋白被活性化合物失活,因此无法将信号传递至 cAMP 通路,从而抑制病菌生长。

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