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The <i>AnUFGT1</i> Is Involved in the Anthurium ‘Alabama’ Anthocyanidin Deficiency
oleh: Zhiying Li, Jiabin Wang, Yu Gao, Yonglin Jing, Junguo Li, Li Xu
Format: | Article |
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Diterbitkan: | MDPI AG 2024-04-01 |
Deskripsi
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 (<i>UF3GT</i>) gene is the key enzyme involved in promoting anthocyanin accumulation through glycosylation downstream of the anthocyanin synthesis pathway (ASP). Abnormal functioning of <i>UFGT</i> usually results in a reduction in or loss of anthocyanins. The aim of this study was to reveal the role of one anthurium <i>UFGT</i> gene (<i>AnUFGT1</i>) 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 <i>Arabidopsis</i> UFGT functionally deficient mutant (ufgt) and ‘X’ validated the function of <i>AnUFGT1</i>. 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 <i>AnUFGT1</i> were significantly greater in ‘Alabama’ than in ‘X’. The overexpression of <i>AnUFGT1</i> in <i>ufgt</i> significantly increased its anthocyanin contents. The overexpression of <i>AnUFGT1</i> in ‘X’, mediated by a new injection method, can only promote the synthesis of trace anthocyanins. These results showed that <i>AnUFGT1</i> could fully compensate the phenotype of <i>ufgt</i>, 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 <i>AnUFGT1</i>, but <i>AnUFGT1</i> is not the only factor. There should be other factors interacting with <i>AnUFGT1</i> that cause anthocyanin deficiency.