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缺氧条件下的基因调控和生存需要淀粉的可用性和代谢。

Gene Regulation and Survival under Hypoxia Requires Starch Availability and Metabolism.

机构信息

Institute of Agricultural Biology and Biotechnology, CNR, National Research Council, 56124 Pisa, Italy.

PlantLab, Institute of Life Sciences, Scuola Superiore Sant'Anna, 56017 San Giuliano Terme (Pisa), Italy.

出版信息

Plant Physiol. 2018 Feb;176(2):1286-1298. doi: 10.1104/pp.17.01002. Epub 2017 Oct 30.

Abstract

Plants respond to hypoxia, often caused by submergence, by expressing a specific set of genes that contribute to acclimation to this unfavorable environmental condition. Genes induced by low oxygen include those encoding enzymes for carbohydrate metabolism and fermentation, pathways that are required for survival. Sugar availability is therefore of crucial importance for energy production under hypoxia. Here, we show that Arabidopsis () plants require starch for surviving submergence as well as for ensuring the rapid induction of genes encoding enzymes required for anaerobic metabolism. The starchless mutant is highly susceptible to submergence and also fails to induce anaerobic genes at the level of the wild type. Treating wild-type plants under conditions inducing sugar starvation results in a weak induction of alcohol dehydrogenase and other anaerobic genes. Induction of gene expression under hypoxia requires transcription factors belonging to group VII ethylene response factors (ERF-VII) that, together with plant Cys oxidases, act as an oxygen-sensing mechanism. We show that repression of this pathway by sugar starvation occurs downstream of the hypoxia-dependent stabilization of ERF-VII proteins and independently of the energy sensor protein kinases SnRK1.1 (SNF1-related kinase 1.1).

摘要

植物通过表达一组特定的基因来应对缺氧,通常是由于淹没造成的,这些基因有助于适应这种不利的环境条件。低氧诱导的基因包括编码碳水化合物代谢和发酵酶的基因,这些途径是生存所必需的。因此,在缺氧条件下,糖的可用性对于能量产生至关重要。在这里,我们表明拟南芥(Arabidopsis)植物需要淀粉来适应淹没,也需要淀粉来确保快速诱导编码厌氧代谢所需酶的基因。淀粉缺失突变体对淹没高度敏感,并且也不能在野生型水平上诱导厌氧基因。在诱导糖饥饿的条件下处理野生型植物会导致酒精脱氢酶和其他厌氧基因的弱诱导。在缺氧下诱导基因表达需要属于乙烯反应因子 VII 组(ERF-VII)的转录因子,这些转录因子与植物半胱氨酸氧化酶一起作为氧气感应机制。我们表明,该途径的抑制作用是通过糖饥饿发生的,糖饥饿发生在 ERF-VII 蛋白的缺氧依赖性稳定之后,并且独立于能量传感器蛋白激酶 SnRK1.1(SNF1 相关激酶 1.1)。

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