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磷脂酰肌醇4激酶激活是拟南芥悬浮细胞对水杨酸的早期反应。

Phosphatidylinositol 4-kinase activation is an early response to salicylic acid in Arabidopsis suspension cells.

作者信息

Krinke Ondrej, Ruelland Eric, Valentová Olga, Vergnolle Chantal, Renou Jean-Pierre, Taconnat Ludivine, Flemr Matyás, Burketová Lenka, Zachowski Alain

机构信息

Université Pierre et Marie Curie-Paris 6 and Centre National de la Recherche Scientifique, Unité Mixte de Recherche 7180, Laboratoire de Physiologie Cellulaire et Moléculaire des Plantes, Ivry-sur-Seine, France.

出版信息

Plant Physiol. 2007 Jul;144(3):1347-59. doi: 10.1104/pp.107.100842. Epub 2007 May 11.

Abstract

Salicylic acid (SA) has a central role in defense against pathogen attack. In addition, its role in such diverse processes as germination, flowering, senescence, and thermotolerance acquisition has been documented. However, little is known about the early signaling events triggered by SA. Using Arabidopsis (Arabidopsis thaliana) suspension cells as a model, it was possible to show by in vivo metabolic phospholipid labeling with (33)P(i) that SA addition induced a rapid and early (in few minutes) decrease in a pool of phosphatidylinositol (PI). This decrease paralleled an increase in PI 4-phosphate and PI 4,5-bisphosphate. These changes could be inhibited by two different inhibitors of type III PI 4-kinases, phenylarsine oxide and 30 microm wortmannin; no inhibitory effect was seen with 1 microm wortmannin, a concentration inhibiting PI 3-kinases but not PI 4-kinases. We therefore undertook a study of the effects of wortmannin on SA-responsive transcriptomes. Using the Complete Arabidopsis Transcriptome MicroArray chip, we could identify 774 genes differentially expressed upon SA treatment. Strikingly, among these genes, the response to SA of 112 of them was inhibited by 30 microm wortmannin, but not by 1 microm wortmannin.

摘要

水杨酸(SA)在抵御病原体攻击中起核心作用。此外,其在种子萌发、开花、衰老和耐热性获得等多种过程中的作用也有文献记载。然而,关于SA引发的早期信号事件却知之甚少。以拟南芥悬浮细胞为模型,通过用(33)P(i)进行体内代谢磷脂标记,发现添加SA会导致磷脂酰肌醇(PI)池迅速且早期(几分钟内)减少。这种减少与PI 4-磷酸和PI 4,5-二磷酸的增加平行。这些变化可被两种不同的III型PI 4-激酶抑制剂氧化苯胂和30微摩尔渥曼青霉素抑制;1微摩尔渥曼青霉素(一种抑制PI 3-激酶而非PI 4-激酶的浓度)未见抑制作用。因此,我们研究了渥曼青霉素对SA响应转录组的影响。使用完整的拟南芥转录组微阵列芯片,我们能够鉴定出774个在SA处理后差异表达的基因。引人注目的是,在这些基因中,112个基因对SA的反应被30微摩尔渥曼青霉素抑制,但未被1微摩尔渥曼青霉素抑制。

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