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乙烯信号通路参与拟南芥幼苗中糖诱导的对除草剂阿特拉津的耐受性。

Involvement of the ethylene-signalling pathway in sugar-induced tolerance to the herbicide atrazine in Arabidopsis thaliana seedlings.

作者信息

Sulmon Cécile, Gouesbet Gwenola, El Amrani Abdelhak, Couée Ivan

机构信息

Centre National de la Recherche Scientifique, Université de Rennes 1, UMR 6553 ECOBIO, Campus de Beaulieu, bâtiment 14A, F-35042 Rennes Cedex, France.

出版信息

J Plant Physiol. 2007 Aug;164(8):1083-92. doi: 10.1016/j.jplph.2006.11.005. Epub 2007 Feb 12.

Abstract

Soluble sugars can induce tolerance to otherwise lethal concentrations of the herbicide atrazine in Arabidopsis thaliana seedlings. This sugar-induced tolerance involves modifications of gene expression which are likely to be related to sugar and xenobiotic signal transduction. Since it has been suggested that ethylene- and sugar-signalling pathways may interact, the effects of glucose (Glc) and sucrose (Suc) on seedling growth and tolerance to atrazine were analysed in etr1-1, ein2-1, ein4, and sis1/ctr1-12 ethylene-signalling mutant backgrounds, where key steps of ethylene signal transduction are affected. Both ethylene-insensitive and ethylene-constitutive types of mutants were found to be affected in sugar-induced chlorophyll accumulation and root growth and in sugar-induced tolerance to atrazine. Interactions between ethylene and sugars were thus shown to take place during enhancement of seedling growth by low-to-moderate (up to 80 mM) sugar concentrations. The strong impairment of sugar-induced atrazine tolerance in etr1-1, ein2-1, and ein4 mutants demonstrated that this tolerance required active signalling pathways and could not be ascribed to mere metabolic effects nor to mere growth enhancement. Sugar-induced atrazine tolerance thus seemed to involve activation by sugar and atrazine of hexokinase-independent sugar signalling pathways and of ethylene signalling pathways, resulting in derepression of hexokinase-mediated Glc repression and in induction of protection mechanisms against atrazine injury.

摘要

可溶性糖可诱导拟南芥幼苗对原本致死浓度的除草剂阿特拉津产生耐受性。这种糖诱导的耐受性涉及基因表达的改变,这可能与糖和外源信号转导有关。由于有人提出乙烯信号通路和糖信号通路可能相互作用,因此在乙烯信号转导关键步骤受到影响的etr1-1、ein2-1、ein4和sis1/ctr1-12乙烯信号突变体背景下分析了葡萄糖(Glc)和蔗糖(Suc)对幼苗生长和阿特拉津耐受性的影响。发现乙烯不敏感型和乙烯组成型突变体在糖诱导的叶绿素积累、根系生长以及糖诱导的阿特拉津耐受性方面均受到影响。因此,在低至中等(高达80 mM)糖浓度促进幼苗生长的过程中,乙烯和糖之间发生了相互作用。etr1-1、ein2-1和ein4突变体中糖诱导的阿特拉津耐受性严重受损表明,这种耐受性需要活跃的信号通路,不能仅仅归因于代谢效应或单纯的生长促进作用。因此,糖诱导的阿特拉津耐受性似乎涉及糖和阿特拉津对不依赖己糖激酶的糖信号通路以及乙烯信号通路的激活,导致己糖激酶介导的葡萄糖抑制作用解除,并诱导针对阿特拉津损伤的保护机制。

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