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脱落酸与糖信号在叶片衰老调控中的相互作用。

Interactions of abscisic acid and sugar signalling in the regulation of leaf senescence.

作者信息

Pourtau Nathalie, Marès Magali, Purdy Sarah, Quentin Nicolas, Ruël Alexandra, Wingler Astrid

机构信息

Department of Biology, University College London, Gower Street, WC1E 6BT, London, UK.

出版信息

Planta. 2004 Sep;219(5):765-72. doi: 10.1007/s00425-004-1279-5. Epub 2004 Apr 29.

Abstract

Leaf senescence can be triggered by a high availability of carbon relative to nitrogen or by external application of abscisic acid (ABA). Most Arabidopsis mutants with decreased sugar sensitivity during early plant development are either ABA insensitive (abi mutants) or ABA deficient (aba mutants). To analyse the interactions of carbon, nitrogen and ABA in the regulation of senescence, wild-type Arabidopsis thaliana (L.) Heynh. and aba and abi mutants were grown on medium with varied glucose and nitrogen supply. On medium containing glucose in combination with low, but not in combination with high nitrogen supply, senescence was accelerated and sucrose, glucose and fructose accumulated strongly. In abi mutants that are not affected in sugar responses during early development (abi1-1 and abi2-1), we observed no difference in the sugar-dependent regulation of senescence compared to wild-type plants. Similarly, senescence was not affected in the sugar-insensitive abi4-1 mutant. In contrast, the abi5-1 mutant did exhibit a delay in senescence compared to its wild type. As ABA has been reported to induce senescence and ABA deficiency results in sugar insensitivity during early development, we expected senescence to be delayed in aba mutants. However, the aba1-1 and aba2-1 mutants showed accelerated senescence compared to their wild types on glucose-containing medium. Our results show that, in contrast to sugar signalling in seedlings, ABA is not required for the sugar-dependent induction of leaf senescence. Instead, increased sensitivity to osmotic stress could have triggered early senescence in the aba mutants.

摘要

叶片衰老可由相对于氮而言较高的碳可用性或通过外源施加脱落酸(ABA)引发。大多数在植物早期发育过程中对糖敏感性降低的拟南芥突变体要么是ABA不敏感型(abi突变体),要么是ABA缺陷型(aba突变体)。为了分析碳、氮和ABA在衰老调控中的相互作用,将野生型拟南芥(L.)Heynh.以及aba和abi突变体在葡萄糖和氮供应不同的培养基上培养。在含有葡萄糖且氮供应低但不是高的培养基上,衰老加速,蔗糖、葡萄糖和果糖大量积累。在早期发育过程中对糖反应无影响的abi突变体(abi1-1和abi2-1)中,与野生型植物相比,我们未观察到糖依赖性衰老调控方面的差异。同样,糖不敏感的abi4-1突变体中的衰老也未受影响。相反,与野生型相比,abi5-1突变体确实表现出衰老延迟。由于据报道ABA可诱导衰老且ABA缺乏会导致早期发育过程中的糖不敏感,我们预期aba突变体中的衰老会延迟。然而,在含葡萄糖的培养基上,aba1-1和aba2-1突变体与野生型相比表现出衰老加速。我们的结果表明,与幼苗中的糖信号传导不同,叶片衰老的糖依赖性诱导不需要ABA。相反,对渗透胁迫敏感性的增加可能触发了aba突变体中的早期衰老。

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