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ABA 介导了枸杞植物发育相关的花青素生物合成和果实着色。

ABA mediates development-dependent anthocyanin biosynthesis and fruit coloration in Lycium plants.

机构信息

National Wolfberry Engineering Research Center, Ningxia Academy of Agriculture and Forestry Sciences, Yinchuan, 750002, China.

College of Life Sciences, Northwest A&F University, Yangling, 712100, Shaanxi, China.

出版信息

BMC Plant Biol. 2019 Jul 15;19(1):317. doi: 10.1186/s12870-019-1931-7.

DOI:10.1186/s12870-019-1931-7
PMID:31307384
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6631627/
Abstract

BACKGROUND

Anthocyanins, which are colored pigments, have long been used as food and pharmaceutical ingredients due to their potential health benefits, but the intermediate signals through which environmental or developmental cues regulate anthocyanin biosynthesis remains poorly understood. Fleshy fruits have become a good system for studying the regulation of anthocyanin biosynthesis, and exploring the mechanism underlying pigment metabolism is valuable for controlling fruit ripening.

RESULTS

The present study revealed that ABA accumulated during Lycium fruit ripening, and this accumulation was positively correlated with the anthocyanin contents and the LbNCED1 transcript levels. The application of exogenous ABA and of the ABA biosynthesis inhibitor fluridon increased and decreased the content of anthocyanins in Lycium fruit, respectively. This is the first report to show that ABA promotes the accumulation of anthocyanins in Lycium fruits. The variations in the anthocyanin content were consistent with the variations in the expression of the genes encoding the MYB-bHLH-WD40 transcription factor complex or anthocyanin biosynthesis-related enzymes. Virus-induced LbNCED1 gene silencing significantly slowed fruit coloration and decreased both anthocyanin and ABA accumulation during Lycium fruit ripening. An qRT-PCR analysis showed that LbNCED1 gene silencing clearly reduced the transcript levels of both structural and regulatory genes in the flavonoid biosynthetic pathway.

CONCLUSIONS

Based on the results, a model of ABA-mediated development-dependent anthocyanin biosynthesis and fruit coloration during Lycium fruit maturation was proposed. In this model, the developmental cues transcriptionally activates LbNCED1 and thus enhances accumulation of the phytohormone ABA, and the accumulated ABA stimulates transcription of the MYB-bHLH-WD40 transcription factor complex to upregulate the expression of structural genes in the flavonoid biosynthetic pathway and thereby promoting anthocyanin production and fruit coloration. Our results provide a valuable strategy that could be used in practice to regulate the ripening and quality of fresh fruit in medicinal and edible plants by modifying the phytohormone ABA.

摘要

背景

花色苷是一种有色的色素,由于其潜在的健康益处,长期以来一直被用作食品和药物成分。但是,环境或发育线索调节花色苷生物合成的中间信号仍然知之甚少。肉质果实已成为研究花色苷生物合成调控的良好体系,探索色素代谢的机制对于控制果实成熟具有重要意义。

结果

本研究表明,ABA 在枸杞果实成熟过程中积累,并且这种积累与花色苷含量和 LbNCED1 转录本水平呈正相关。外源 ABA 的应用和 ABA 生物合成抑制剂 fluridon 的应用分别增加和减少了枸杞果实中花色苷的含量。这是第一个报道表明 ABA 促进枸杞果实中花色苷积累的报告。花色苷含量的变化与编码 MYB-bHLH-WD40 转录因子复合物或花色苷生物合成相关酶的基因的表达变化一致。病毒诱导的 LbNCED1 基因沉默显著减缓了果实着色,并减少了枸杞果实成熟过程中花色苷和 ABA 的积累。qRT-PCR 分析表明,LbNCED1 基因沉默明显降低了类黄酮生物合成途径中结构基因和调节基因的转录水平。

结论

基于这些结果,提出了一个 ABA 介导的发育依赖性花色苷生物合成和枸杞果实成熟过程中果实着色的模型。在该模型中,发育线索转录激活 LbNCED1,从而增强植物激素 ABA 的积累,积累的 ABA 刺激 MYB-bHLH-WD40 转录因子复合物的转录,上调类黄酮生物合成途径中结构基因的表达,从而促进花色苷的产生和果实着色。我们的结果提供了一种有价值的策略,可以通过修饰植物激素 ABA 来调节药用和食用植物的果实成熟和品质。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0704/6631627/969a3eab9477/12870_2019_1931_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0704/6631627/7e64da2d3e63/12870_2019_1931_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0704/6631627/037de59ba040/12870_2019_1931_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0704/6631627/901426f34796/12870_2019_1931_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0704/6631627/04ac90f07428/12870_2019_1931_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0704/6631627/e4448205da90/12870_2019_1931_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0704/6631627/6f59adc78f45/12870_2019_1931_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0704/6631627/d9c15a3bf4e6/12870_2019_1931_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0704/6631627/969a3eab9477/12870_2019_1931_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0704/6631627/7e64da2d3e63/12870_2019_1931_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0704/6631627/037de59ba040/12870_2019_1931_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0704/6631627/901426f34796/12870_2019_1931_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0704/6631627/04ac90f07428/12870_2019_1931_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0704/6631627/e4448205da90/12870_2019_1931_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0704/6631627/6f59adc78f45/12870_2019_1931_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0704/6631627/d9c15a3bf4e6/12870_2019_1931_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0704/6631627/969a3eab9477/12870_2019_1931_Fig8_HTML.jpg

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