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以锌依赖的方式控制磷酸盐的动态平衡。

controls phosphate homeostasis in a zinc-dependent manner.

机构信息

BPMP, Univ Montpellier, CNRS, INRA, SupAgro, Montpellier, France.

Laboratory of Genetics, Wageningen University, Wageningen, Netherlands.

出版信息

Elife. 2018 Feb 17;7:e32077. doi: 10.7554/eLife.32077.

Abstract

All living organisms require a variety of essential elements for their basic biological functions. While the homeostasis of nutrients is highly intertwined, the molecular and genetic mechanisms of these dependencies remain poorly understood. Here, we report a discovery of a molecular pathway that controls phosphate (Pi) accumulation in plants under Zn deficiency. Using genome-wide association studies, we first identified allelic variation of the () gene as the key determinant of shoot Pi accumulation under Zn deficiency. We then show that regulatory variation at the LPCAT1 locus contributes significantly to this natural variation and we further demonstrate that the regulation of expression involves bZIP23 TF, for which we identified a new binding site sequence. Finally, we show that in Zn deficient conditions loss of function of increases the phospholipid Lyso-PhosphatidylCholine/PhosphatidylCholine ratio, the expression of the Pi transporter PHT1;1, and that this leads to shoot Pi accumulation.

摘要

所有生物体的基本生物功能都需要多种必需元素。尽管营养物质的动态平衡高度交织在一起,但这些依赖性的分子和遗传机制仍知之甚少。在这里,我们报告了一个发现,即在锌缺乏下控制植物中磷酸盐(Pi)积累的分子途径。使用全基因组关联研究,我们首先确定了()基因的等位基因变异是缺锌条件下 shoot Pi 积累的关键决定因素。然后我们表明,LPCAT1 基因座的调节变异对此自然变异有重要贡献,我们进一步证明,对表达的调控涉及 bZIP23 TF,我们为此鉴定了一个新的结合位点序列。最后,我们表明在锌缺乏条件下,功能丧失增加了磷脂 Lyso-PhosphatidylCholine/PhosphatidylCholine 比率,Pi 转运蛋白 PHT1;1 的表达,这导致 shoot Pi 积累。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7eb/5826268/b2c44ded1589/elife-32077-fig1.jpg

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