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The AnUFGT1 Is Involved in the Anthurium 'Alabama' Anthocyanidin Deficiency

文献类型： 外文期刊

作者： Li, Zhiying 1 ; Wang, Jiabin 1 ; Gao, Yu 1 ; Jing, Yonglin 1 ; Li, Junguo 1 ; Xu, Li 1 ;

作者机构： 1.Chinese Acad Trop Agr Sci, Inst Trop Crop Genet Resources, Haikou 571101, Peoples R China

2.Minist Agr, Key Lab Crop Gene Resources & Germplasm Enhancemen, Danzhou 571700, Peoples R China

3.Natl Gene Bank Trop Crops, Hainan Prov Key Lab Trop Crops Germplasm Resources, Danzhou 571700, Peoples R China

关键词： anthurium; metabolome analysis; UDP glucose-flavonoid 3-O-glucosyltransferase; genetic transformation

期刊名称：HORTICULTURAE （ 影响因子：3.1； 五年影响因子：3.4 ）

ISSN：

年卷期： 2024 年 10 卷 4 期

页码：

收录情况： SCI

摘要： Anthurium is the second largest tropical flower crop in the world. The international market has urgent demand for anthurium varieties with different spathe colors, which mainly arises from the types and contents of anthocyanin. The flavonoid 3-O-glycosyltransferase (UF3GT) gene is the key enzyme involved in promoting anthocyanin accumulation through glycosylation downstream of the anthocyanin synthesis pathway (ASP). Abnormal functioning of UFGT usually results in a reduction in or loss of anthocyanins. The aim of this study was to reveal the role of one anthurium UFGT gene (AnUFGT1) in 'Xueyu' (X), an anthocyanin-deficient mutant of 'Alabama'. Metabolome analysis was used to analyze the metabolic products in the ASP to determine the possible key link of the anthocyanin deletion mutation. Agrobacterium-mediated transformation of Arabidopsis UFGT functionally deficient mutant (ufgt) and 'X' validated the function of AnUFGT1. The results of comparative metabolome analysis of 'X' and 'Alabama' showed that there was no significant difference in product levels upstream of ASP. The expression levels of AnUFGT1 were significantly greater in 'Alabama' than in 'X'. The overexpression of AnUFGT1 in ufgt significantly increased its anthocyanin contents. The overexpression of AnUFGT1 in 'X', mediated by a new injection method, can only promote the synthesis of trace anthocyanins. These results showed that AnUFGT1 could fully compensate the phenotype of ufgt, but only partially compensate the anthocyanidin-deficient phenotype of anthurium mutant X. This difference suggested that anthocyanin-deletion mutations in anthurium 'X' are associated with AnUFGT1, but AnUFGT1 is not the only factor. There should be other factors interacting with AnUFGT1 that cause anthocyanin deficiency.

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