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一般控制不可抑制 4 降解 14-3-3 和 RIN4 复合物来调节气孔开度,这对非寄主疾病抗性和耐旱性有影响。

GENERAL CONTROL NONREPRESSIBLE4 Degrades 14-3-3 and the RIN4 Complex to Regulate Stomatal Aperture with Implications on Nonhost Disease Resistance and Drought Tolerance.

机构信息

Noble Research Institute, Ardmore, Oklahoma 73401.

Noble Research Institute, Ardmore, Oklahoma 73401

出版信息

Plant Cell. 2017 Sep;29(9):2233-2248. doi: 10.1105/tpc.17.00070. Epub 2017 Aug 30.

DOI:10.1105/tpc.17.00070
PMID:28855332
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5635975/
Abstract

Plants have complex and adaptive innate immune responses against pathogen infections. Stomata are key entry points for many plant pathogens. Both pathogens and plants regulate stomatal aperture for pathogen entry and defense, respectively. Not all plant proteins involved in stomatal aperture regulation have been identified. Here, we report GENERAL CONTROL NONREPRESSIBLE4 (GCN4), an AAA-ATPase family protein, as one of the key proteins regulating stomatal aperture during biotic and abiotic stress. Silencing of in and compromises host and nonhost disease resistance due to open stomata during pathogen infection. overexpression plants have reduced H-ATPase activity, stomata that are less responsive to pathogen virulence factors such as coronatine (phytotoxin produced by the bacterium ) or fusicoccin (a fungal toxin produced by the fungus ), reduced pathogen entry, and enhanced drought tolerance. This study also demonstrates that AtGCN4 interacts with RIN4 and 14-3-3 proteins and suggests that GCN4 degrades RIN4 and 14-3-3 proteins via a proteasome-mediated pathway and thereby reduces the activity of the plasma membrane H-ATPase complex, thus reducing proton pump activity to close stomata.

摘要

植物具有复杂而适应性强的先天免疫反应来抵御病原体感染。气孔是许多植物病原体的主要进入点。病原体和植物分别调节气孔开度以利于病原体进入和防御。并非所有参与气孔开度调节的植物蛋白都已被鉴定。在这里,我们报告 GENERAL CONTROL NONREPRESSIBLE4(GCN4),一种 AAA-ATPase 家族蛋白,作为调节生物和非生物胁迫期间气孔开度的关键蛋白之一。由于在病原体感染期间气孔开放,沉默 和 会损害宿主和非宿主的疾病抗性。过表达植物的 H-ATPase 活性降低,气孔对病原体毒力因子(如由细菌产生的植物毒素 coronatine 或由真菌产生的真菌毒素 fusicoccin)的反应性降低,病原体进入减少,耐旱性增强。这项研究还表明,AtGCN4 与 RIN4 和 14-3-3 蛋白相互作用,并表明 GCN4 通过蛋白酶体介导的途径降解 RIN4 和 14-3-3 蛋白,从而降低质膜 H-ATPase 复合物的活性,从而减少质子泵活动以关闭气孔。

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