Cit1,2RhaT and two novel CitdGlcTs participate in flavor-related flavonoid metabolism during citrus fruit development

文献类型： 外文期刊

第一作者： Chen, Jiajing

作者： Chen, Jiajing;Yuan, Ziyu;Zhang, Haipeng;Li, Wenyun;Shi, Meiyan;Peng, Zhaoxin;Li, Mingyue;Tian, Jing;Deng, Xiuxin;Cheng, Yunjiang;Xie, Zongzhou;Xu, Juan;Deng, Cecilia Hong;Yao, Jia-Long;Li, Wenyun;Zeng, Jiwu

作者机构：

关键词： Bitterness; citrus; flavonoid; flavonoid-7-O-di-glucosides; flavonoid-7-O-glucoside; neohesperidoside

期刊名称：JOURNAL OF EXPERIMENTAL BOTANY （ 影响因子：6.992； 五年影响因子：7.86 ）

ISSN： 0022-0957

年卷期： 2019 年 70 卷 10 期

页码：

收录情况： SCI

摘要： Neohesperidosides are disaccharides that are present in some flavonoids and impart a bitter taste, which can significantly affect the commercial value of citrus fruits. In this study, we identified three flavonoid-7-O-di-glucosyltransferase (dGlcT) genes closely related to 1,2-rhamnosyltransferase (1,2RhaT) in citrus genomes. However, only 1,2RhaT was directly linked to the accumulation of neohesperidoside, as demonstrated by association analysis of 50 accessions and co-segregation analysis of an F-1 population derived from Citrus reticulata x Poncirus trifoliata. In transgenic tobacco BY2 cells, over-expression of CitdGlcTs resulted in flavonoid-7-O-glucosides being catalysed into bitterless flavonoid-7-O-di-glucosides, whereas over-expression of Cit1,2RhaT converted the same substrate into bitter-tasting flavonoid-7-O-neohesperidoside. Unlike 1,2RhaT, during citrus fruit development the dGlcTs showed an opposite expression pattern to CHS and CHI, two genes encoding rate-limiting enzymes of flavonoid biosynthesis. An uncoupled availability of dGlcTs and substrates might result in trace accumulation of flavonoid-7-O-di-glucosides in the fruit of C. maxima (pummelo). Past human selection of the deletion and functional mutation of 1,2RhaT has led step-by-step to the evolution of the flavor-related metabolic network in citrus. Our research provides the basis for potentially improving the taste in citrus fruit through manipulation of the network by knocking-out 1,2RhaT or by enhancing the expression of dGlcT using genetic transformation.

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