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花生过敏原基因 Ara h 3 在发育胚胎中的表观遗传调控。

Epigenetic regulation of peanut allergen gene Ara h 3 in developing embryos.

机构信息

School of Life Sciences, Sun Yat-Sen University, Guangzhou, China.

出版信息

Planta. 2010 Apr;231(5):1049-60. doi: 10.1007/s00425-010-1111-3. Epub 2010 Feb 16.

Abstract

Peanut (Arachis hypogaea) allergy is one of the most serious food allergies. Peanut seed protein, Ara h 3, is considered to be one of the most important peanut allergens. Little is known about the temporal and spatial regulation mechanism of Ara h 3 during seed development. In this study, chromatin structure of the Ara h 3 promoter was analyzed to examine its transcriptional regulation. Analysis of transgenic plants of Arabidopsis thaliana expressing Arah3: GUS showed that the Ara h 3 promoter could efficiently direct the seed-specific expression of the GUS reporter gene. Chromatin immunoprecipitation revealed that nucleosomes were depleted at the core promoter of the Ara h 3 upon full activation in the late stage of embryo maturation, which was accompanied by a dramatic decrease of histone acetylation. However, in the early stage of embryo maturation, histone H3 hyperacetylation at the core promoter of Ara h 3 was detected. A decrease of histone H3-K9 dimethylation levels at core promoter of Ara h 3 was also observed with concomitant repression of Ara h 3 in the vegetative tissues. Our results suggest that the histone modification status of Ara h 3 undergoes targeted changes including the increase of histone H3 acetylation and decrease of histone H3-K9 dimethylation in early maturation embryos. In addition, the loss of histone H3 from the proximal promoter of Ara h 3 is associated with its high expression during late embryo maturation.

摘要

花生(Arachis hypogaea)过敏是最严重的食物过敏之一。花生种子蛋白 Ara h 3 被认为是最重要的花生过敏原之一。目前对于 Ara h 3 在种子发育过程中的时空调控机制知之甚少。本研究分析了 Ara h 3 启动子的染色质结构,以研究其转录调控。对表达 Arah3:GUS 的拟南芥转基因植物的分析表明,Ara h 3 启动子可以有效地指导 GUS 报告基因在种子中的特异性表达。染色质免疫沉淀显示,在胚胎成熟后期完全激活时,Ara h 3 的核心启动子处的核小体被耗尽,同时组蛋白乙酰化急剧下降。然而,在胚胎成熟的早期阶段,检测到 Ara h 3 核心启动子处的组蛋白 H3 高度乙酰化。在营养组织中同时抑制 Ara h 3 时,也观察到 Ara h 3 核心启动子处组蛋白 H3-K9 二甲基化水平降低。我们的结果表明,Ara h 3 的组蛋白修饰状态发生了靶向变化,包括早期成熟胚胎中组蛋白 H3 乙酰化增加和组蛋白 H3-K9 二甲基化减少。此外,Ara h 3 近端启动子处组蛋白 H3 的丢失与其在晚期胚胎成熟过程中的高表达有关。

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