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拟南芥糖信号突变体对外源脯氨酸施用的超敏反应。

Hypersensitivity of an Arabidopsis sugar signaling mutant toward exogenous proline application.

作者信息

Hellmann H, Funck D, Rentsch D, Frommer W B

机构信息

Pflanzenphysiologie, Zentrum für Molekularbiologie der Pflanzen, Universität Tübingen, D-72076 Tübingen, Germany.

出版信息

Plant Physiol. 2000 Feb;122(2):357-68. doi: 10.1104/pp.122.2.357.

Abstract

In transgenic Arabidopsis a patatin class I promoter from potato is regulated by sugars and proline (Pro), thus integrating signals derived from carbon and nitrogen metabolism. In both cases a signaling cascade involving protein phosphatases is involved in induction. Other endogenous genes are also regulated by both Pro and carbohydrates. Chalcone synthase (CHS) gene expression is induced by both, whereas the Pro biosynthetic Delta(1)-pyrroline-5-carboxylate synthetase (P5CS) is induced by high Suc concentrations but repressed by Pro, and Pro dehydrogenase (ProDH) is inversely regulated. The mutant rsr1-1, impaired in sugar dependent induction of the patatin promoter, is hypersensitive to low levels of external Pro and develops autofluorescence and necroses. Toxicity of Pro can be ameliorated by salt stress and exogenously supplied metabolizable carbohydrates. The rsr1-1 mutant shows a reduced response regarding sugar induction of CHS and P5CS expression. ProDH expression is de-repressed in the mutant but still down-regulated by sugar. Pro toxicity seems to be mediated by the degradation intermediate Delta(1)-pyrroline-5-carboxylate. Induction of the patatin promoter by carbohydrates and Pro, together with the Pro hypersensitivity of the mutant rsr1-1, demonstrate a new link between carbon/nitrogen and stress responses.

摘要

在转基因拟南芥中,来自马铃薯的I类patatin启动子受糖类和脯氨酸(Pro)调控,从而整合来自碳代谢和氮代谢的信号。在这两种情况下,涉及蛋白磷酸酶的信号级联反应参与诱导过程。其他内源基因也受Pro和碳水化合物的调控。查尔酮合酶(CHS)基因的表达受二者诱导,而Pro生物合成途径中的Δ¹-吡咯啉-5-羧酸合成酶(P5CS)受高浓度蔗糖诱导,但受Pro抑制,脯氨酸脱氢酶(ProDH)则受到相反的调控。突变体rsr1-1在patatin启动子的糖依赖性诱导方面存在缺陷,对低水平的外源Pro高度敏感,并出现自发荧光和坏死现象。Pro的毒性可通过盐胁迫和外源供应的可代谢碳水化合物得到缓解。rsr1-1突变体在CHS和P5CS表达的糖诱导方面表现出反应降低。ProDH的表达在突变体中去抑制,但仍受糖的下调。Pro毒性似乎是由降解中间产物Δ¹-吡咯啉-5-羧酸介导的。碳水化合物和Pro对patatin启动子的诱导,以及突变体rsr1-1对Pro的超敏感性,证明了碳/氮与胁迫反应之间的新联系。

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