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乙烯激活 PpERF105 诱导抑制型 R2R3-MYB 基因 PpMYB140 的表达,从而抑制红皮梨果实中花色苷的生物合成。

Ethylene-activated PpERF105 induces the expression of the repressor-type R2R3-MYB gene PpMYB140 to inhibit anthocyanin biosynthesis in red pear fruit.

机构信息

Department of Horticulture, Zhejiang University, Hangzhou, Zhejiang, 310058, PR China.

Zhejiang Provincial Key Laboratory of Integrative Biology of Horticultural Plants, Hangzhou, Zhejiang, 310058, PR China.

出版信息

Plant J. 2021 Jan;105(1):167-181. doi: 10.1111/tpj.15049. Epub 2020 Nov 21.

Abstract

Ethylene induces anthocyanin biosynthesis in most fruits, including apple (Malus domestica), strawberry (Fragaria × ananassa), and plum (Prunus spp.). However, ethylene inhibits anthocyanin biosynthesis in pear (Pyrus spp.), but the underlying molecular mechanism has not been characterized. In this study, ethylene induced the expression of PpERF105, which encodes a transcription factor. PpERF105 functioned as a transcriptional activator, but it inhibited anthocyanin biosynthesis in pear. A transcriptome analysis revealed that PpERF105 activated the expression of PpMYB140, which encodes an R2R3-MYB transcriptional repressor. Moreover, PpMYB140 directly inhibited the expression of anthocyanin-related structural genes. It also competed with PpMYB114 for the binding to bHLH3, ultimately resulting in the formation of the MYB140-bHLH-WDR complex rather than the conventional MBW complex, thereby further inhibiting anthocyanin biosynthesis. Furthermore, PpMYB140 prevented the overaccumulation of anthocyanins in the absence of ethylene. Collectively, our study data indicate that ethylene-induced PpERF105 inhibits anthocyanin biosynthesis by upregulating PpMYB140 expression. Our findings may be useful for elucidating the molecular basis of the ethylene-mediated inhibition of anthocyanin biosynthesis in fruit.

摘要

乙烯在大多数水果中诱导花色苷生物合成,包括苹果(Malus domestica)、草莓(Fragaria × ananassa)和李子(Prunus spp.)。然而,乙烯抑制了梨(Pyrus spp.)中花色苷的生物合成,但潜在的分子机制尚未确定。在这项研究中,乙烯诱导了编码转录因子的 PpERF105 的表达。PpERF105 作为转录激活因子起作用,但它抑制了梨中花色苷的生物合成。转录组分析表明,PpERF105 激活了编码 R2R3-MYB 转录抑制子的 PpMYB140 的表达。此外,PpMYB140 直接抑制花色苷相关结构基因的表达。它还与 PpMYB114 竞争与 bHLH3 的结合,最终形成 MYB140-bHLH-WDR 复合物,而不是常规的 MBW 复合物,从而进一步抑制花色苷的生物合成。此外,PpMYB140 防止了在没有乙烯的情况下花色苷的过度积累。总的来说,我们的研究数据表明,乙烯诱导的 PpERF105 通过上调 PpMYB140 的表达来抑制花色苷的生物合成。我们的发现可能有助于阐明乙烯介导的花色苷生物合成抑制在果实中的分子基础。

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