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拟南芥 GCN2 激酶有助于 ABA 稳态和气孔免疫。

Arabidopsis GCN2 kinase contributes to ABA homeostasis and stomatal immunity.

机构信息

1Department of Biology, University of Alabama at Birmingham, 1300 University Blvd., Birmingham, AL 35294 USA.

Present Address: Bayer Crop Science, 800 N Lindbergh Blvd., Creve Coeur, MO 63144 USA.

出版信息

Commun Biol. 2019 Aug 8;2:302. doi: 10.1038/s42003-019-0544-x. eCollection 2019.

DOI:10.1038/s42003-019-0544-x
PMID:31428690
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6687712/
Abstract

General Control Non-derepressible 2 (GCN2) is an evolutionarily conserved serine/threonine kinase that modulates amino acid homeostasis in response to nutrient deprivation in yeast, human and other eukaryotes. However, the GCN2 signaling pathway in plants remains largely unknown. Here, we demonstrate that in Arabidopsis, bacterial infection activates AtGCN2-mediated phosphorylation of eIF2α and promotes TBF1 translational derepression. Consequently, TBF1 regulates a subset of abscisic acid signaling components to modulate pre-invasive immunity. We show that GCN2 fine-tunes abscisic acid accumulation and signaling during both pre-invasive and post-invasive stages of an infection event. Finally, we also demonstrate that AtGCN2 participates in signaling triggered by phytotoxin coronatine secreted by . . During the preinvasive phase, AtGCN2 regulates stomatal immunity by affecting pathogen-triggered stomatal closure and coronatine-mediated stomatal reopening. Our conclusions support a conserved role of GCN2 in various forms of immune responses across kingdoms, highlighting GCN2's importance in studies on both plant and mammalian immunology.

摘要

一般控制不可诱导 2(GCN2)是一种进化上保守的丝氨酸/苏氨酸激酶,可在酵母、人类和其他真核生物中响应营养缺乏调节氨基酸稳态。然而,植物中的 GCN2 信号通路在很大程度上仍然未知。在这里,我们证明在拟南芥中,细菌感染激活 AtGCN2 介导的 eIF2α磷酸化,并促进 TBF1 的翻译去阻遏。因此,TBF1 调节一组脱落酸信号成分来调节侵入前免疫。我们表明 GCN2 在感染事件的侵入前和侵入后阶段精细调节脱落酸的积累和信号转导。最后,我们还证明 AtGCN2 参与由 分泌的植物毒素冠菌素触发的信号转导。在侵入前阶段,AtGCN2 通过影响病原体触发的气孔关闭和冠菌素介导的气孔重新开放来调节气孔免疫。我们的结论支持 GCN2 在不同形式的免疫反应中在各个领域的保守作用,突出了 GCN2 在植物和哺乳动物免疫学研究中的重要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc9e/6687712/c2097a7d3855/42003_2019_544_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc9e/6687712/33f663f039d4/42003_2019_544_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc9e/6687712/3e9483efba86/42003_2019_544_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc9e/6687712/b1585aa6342a/42003_2019_544_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc9e/6687712/f472ebc37e08/42003_2019_544_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc9e/6687712/c2097a7d3855/42003_2019_544_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc9e/6687712/33f663f039d4/42003_2019_544_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc9e/6687712/3e9483efba86/42003_2019_544_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc9e/6687712/b1585aa6342a/42003_2019_544_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc9e/6687712/f472ebc37e08/42003_2019_544_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc9e/6687712/c2097a7d3855/42003_2019_544_Fig5_HTML.jpg

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