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水杨酸通过抑制生长素信号通路来抑制植物病原体的生长。

Salicylic acid inhibits pathogen growth in plants through repression of the auxin signaling pathway.

作者信息

Wang Dong, Pajerowska-Mukhtar Karolina, Culler Angela Hendrickson, Dong Xinnian

机构信息

Department of Biology, Duke University, Durham, North Carolina 27708, USA.

出版信息

Curr Biol. 2007 Oct 23;17(20):1784-90. doi: 10.1016/j.cub.2007.09.025. Epub 2007 Oct 4.

Abstract

The phytohormone auxin regulates almost every aspect of plant development. At the molecular level, auxin induces gene expression through direct physical interaction with the TIR1-like F box proteins, which in turn remove the Aux/IAA family of transcriptional repressors [1-4]. A growing body of evidence indicates that many plant pathogens can either produce auxin themselves or manipulate host auxin biosynthesis to interfere with the host's normal developmental processes [5-11]. In response, plants probably evolved mechanisms to repress auxin signaling during infection as a defense strategy. Plants overaccumulating the defense signal molecule salicylic acid (SA) frequently display morphological phenotypes that are reminiscent of auxin-deficient or auxin-insensitive mutants, indicating that SA might interfere with auxin responses. By using the Affymetrix ATH1 GeneChip for Arabidopsis thaliana, we performed a comprehensive study of the effects of SA on auxin signaling [12]. We found that SA causes global repression of auxin-related genes, including the TIR1 receptor gene, resulting in stabilization of the Aux/IAA repressor proteins and inhibition of auxin responses. We demonstrate that this inhibitory effect on auxin signaling is a part of the SA-mediated disease-resistance mechanism.

摘要

植物激素生长素几乎调控着植物发育的各个方面。在分子水平上,生长素通过与类TIR1 F盒蛋白直接物理相互作用来诱导基因表达,而类TIR1 F盒蛋白反过来会去除转录抑制因子Aux/IAA家族[1-4]。越来越多的证据表明,许多植物病原体要么自身产生生长素,要么操纵宿主生长素生物合成以干扰宿主的正常发育过程[5-11]。作为一种防御策略,植物可能进化出了在感染期间抑制生长素信号传导的机制。过量积累防御信号分子水杨酸(SA)的植物常常表现出类似于生长素缺陷型或生长素不敏感型突变体的形态表型,这表明SA可能会干扰生长素反应。通过使用针对拟南芥的Affymetrix ATH1基因芯片,我们对SA对生长素信号传导的影响进行了全面研究[12]。我们发现SA会导致生长素相关基因的整体抑制,包括TIR1受体基因,从而使Aux/IAA抑制蛋白稳定并抑制生长素反应。我们证明,这种对生长素信号传导的抑制作用是SA介导的抗病机制的一部分。

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