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Inhibition of FvMYB10 transcriptional activity promotes color loss in strawberry fruit

机译:FVMYB10转录活性的抑制促进了草莓果实中的色损

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FvMYB10 protein has been proved to be a transcriptional switch for anthocyanin biosynthesis in strawberry. A single nucleotide mutation in R2 domain of FvMYB10, named as FvmMYB10, is found to be responsible for the white color in strawberry variety 'Yellow Wonder'. However, the mechanism of FvmMYB10 suppresses anthocyanin biosynthesis in strawberry is largely unknown. Here, we show that the transcriptional level of FvMYB10 and key enzyme genes involved in anthocyanin biosynthesis in 'Yellow Wonder' were lower than that in red color variety `Ruegen', especially at turning to ripening stage. The low expression level of FvmMYBIO may due to his inability to bind to its promoter region and activate its own expression. We found FvMYB10-overexpressing, but not FvmMYBIO-overexpressing, promote anthocyanin accumulation in Arabidopsis and strawberry fruit despite of their similar expression levels. In addition, subcellular localization assay indicated that FvMYB10-YFP, but not FvmMYB10-YFP, localized to sub-nucleus foci (speckles) in the nucleus, implying the mutation of FvMYB10 might inhibit its transcription factor activity and eventually interfere with its function. Subsequently, we confirmed that FvMYB10 bind to the promoter region of some specific key enzyme genes, including FvCHS2 and FvDFR1 and activated their expression. While FvmMYB10 failed to binding and transcriptional activating these genes. Our findings provide insights into molecular mechanism of anthocyanin biosynthesis regulated by MYB10 in strawberry fruits.
机译:已被证明FVMYB10蛋白是草莓中花青素生物合成的转录开关。 FVMYB10的R2结构域中的单个核苷酸突变被发现名为FVMMYB10,该突变将负责草莓品种“黄色奇迹”中的白色颜色。然而,FVMMYB10的机制抑制了草莓中的花青素生物合成在很大程度上。在这里,我们表明,“黄色奇迹”中涉及的FVMYB10和关键酶基因的转录水平低于红色品种“ruegen”,特别是转向成熟阶段。 FVMMYBIO的低表达水平可能是由于他无法与其启动子区域结合并激活其自己的表达。我们发现FVMYB10过度表达,但不是FVMMYBIO过度抑制,尽管它们存在类似的表达水平,但尽管存在类似的表达水平,但促进拟南芥和草莓果实中的花青素积累。此外,亚细胞定位测定表明,FVMYB10-YFP,但不是核心的FVMMYB10-YFP,暗集核心焦点(斑点)暗示FVMYB10的突变可能抑制其转录因子活性,并最终干扰其功能。随后,我们证实FVMYB10与一些特定关键酶基因的启动子区结合,包括FVCHS2和FVDFR1并活化它们的表达。虽然FVMMYB10未能结合和转录激活这些基因。我们的研究结果提供了对草莓果实中MyB10调节的花青素生物合成的分子机制的见解。

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