LSU network hubs integrate abiotic and biotic stress responses via interaction with the superoxide dismutase FSD2.

LSU network hubs integrate abiotic and biotic stress responses via interaction with the superoxide dismutase FSD2.
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DOI:
10.1093/jxb/erw498
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发表时间:
2017-02-01
影响因子:
6.9
通讯作者:
Falter-Braun P
Falter-Braun P
中科院分区:
生物学1区
文献类型:
--
作者:
Garcia-Molina A;Altmann M;Alkofer A;Epple PM;Dangl JL;Falter-Braun P

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低分子量low SULPHUR upreated (LSU)网络枢纽通过刺激活性氧的产生介导几种非生物胁迫条件下的气孔关闭;细菌毒力效应物干扰这一功能。在自然环境中,植物经常同时经历不同的胁迫,不利的非生物条件会削弱植物的免疫系统。相互作用组图谱显示,低硫上调(LSU)蛋白是拟南芥蛋白相互作用网络的枢纽,是来自进化多样化病原体的毒力效应物的目标。在这里,我们发现LSU蛋白在几种非生物和生物胁迫条件下,如营养枯竭或盐胁迫,通过转录和翻译后机制上调。在硫胁迫下,干扰LSU的表达会阻止叶绿体活性氧(ROS)的产生和气孔的正常关闭。我们证明LSU1与叶绿体超氧化物歧化酶FSD2相互作用,并在体内和体外刺激其酶活性。丁香假单胞菌的毒力效应会干扰这种相互作用,并阻止LSU1在叶绿体上的重新定位。我们证明,LSU水平降低会导致暴露于非生物胁迫(如营养缺乏、高盐度或重金属中毒)的植物的疾病易感性适度增强,而LSU1过表达在这些条件下会赋予植物显著的抗病能力。我们的数据表明,网络集线器LSU1在协调植物在非生物胁迫条件下的免疫反应中起着重要作用。
The low molecular weight LOW SULPHUR UPREGULATED (LSU) network hubs mediate stomatal closure during several abiotic stress conditions by stimulating reactive oxygen species production; bacterial virulence effectors interfere with this function. In natural environments, plants often experience different stresses simultaneously, and adverse abiotic conditions can weaken the plant immune system. Interactome mapping revealed that the LOW SULPHUR UPREGULATED (LSU) proteins are hubs in an Arabidopsis protein interaction network that are targeted by virulence effectors from evolutionarily diverse pathogens. Here we show that LSU proteins are up-regulated in several abiotic and biotic stress conditions, such as nutrient depletion or salt stress, by both transcriptional and post-translational mechanisms. Interference with LSU expression prevents chloroplastic reactive oxygen species (ROS) production and proper stomatal closure during sulphur stress. We demonstrate that LSU1 interacts with the chloroplastic superoxide dismutase FSD2 and stimulates its enzymatic activity in vivo and in vitro. Pseudomonas syringae virulence effectors interfere with this interaction and preclude re-localization of LSU1 to chloroplasts. We demonstrate that reduced LSU levels cause a moderately enhanced disease susceptibility in plants exposed to abiotic stresses such as nutrient deficiency, high salinity, or heavy metal toxicity, whereas LSU1 overexpression confers significant disease resistance in several of these conditions. Our data suggest that the network hub LSU1 plays an important role in co-ordinating plant immune responses across a spectrum of abiotic stress conditions.