AtRbohF is a crucial modulator of defence-associated metabolism and a key actor in the interplay between intracellular oxidative stress and pathogenesis responses in Arabidopsis

AtRbohF is a crucial modulator of defence-associated metabolism and a key actor in the interplay between intracellular oxidative stress and pathogenesis responses in Arabidopsis
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DOI:
10.1111/j.1365-313x.2011.04816.x
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发表时间:
2012-02-01
期刊:
影响因子:
7.2
通讯作者:
Noctor, Graham
Noctor, Graham
中科院分区:
生物学1区
文献类型:
--
作者:
Chaouch, Sejir;Queval, Guillaume;Noctor, Graham

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本研究研究了AtRbohD和AtRbohF在三种相互作用中对防御相关代谢的调节作用:(i)与syringae假单胞菌不相容和(ii)相容相互作用;(iii)过氧化氢酶缺乏的cat2背景下的细胞内氧化应激。在所有三种情况下,任何一个基因功能的丧失都会调节防御化合物的反应。AtRbohF基因的功能是水杨酸在相容和不相容相互作用中快速和充分诱导水杨酸(SA)的必要条件,也是对有毒细菌的抗性所必需的。这两种突变都调节了cat2背景下细胞内ROS的作用,尽管主要作用是由atrbohF介导的。该基因功能的缺失增加了cat2中病变的形成,但与cat2触发的SA和camalexin的诱导、谷胱甘肽的积累和抗病性相分离,所有这些在cat2 artbohF中都比在cat2中低得多。三种相互作用产生的GC-TOF-MS谱的详细比较显示,在野生型背景下,cat2效应与细菌感染产生的效应之间存在相当大的重叠。分析两种AtRbohF突变对这些谱的影响提供了进一步的证据,证明AtRbohF与细胞内氧化应激密切相互作用,以调节感染期间的动态代谢反应。因此,AtRbohF似乎不仅在hr相关的细胞死亡中起关键作用,而且在调节代谢反应和耐药性中也起关键作用。基于这三种相互作用的结果,提出了NADPH氧化酶和细胞内ROS如何相互作用以决定病原体防御反应结果的模型。
This work investigated the contribution of AtRbohD and AtRbohF to regulating defence-associated metabolism during three types of interaction: (i) incompatible and (ii) compatible interaction with Pseudomonas syringae; and (iii) intracellular oxidative stress in the catalase-deficient cat2 background. In all three cases, loss of function of either gene modulated the response of defence compounds. AtRbohF gene function was necessary for rapid and full induction of salicylic acid (SA) during compatible and incompatible interactions, and for resistance to virulent bacteria. Both artrboh mutations modulated the effects of intracellular ROS in the cat2 background, although the predominant effect was mediated by atrbohF. Loss of this gene function increased lesion formation in cat2 but uncoupled this effect from cat2-triggered induction of SA and camalexin, accumulation of glutathione and disease resistance, all of which were much lower in cat2 artbohF than in cat2. A detailed comparison of GC-TOF-MS profiles produced by the three interactions revealed considerable overlap between cat2 effects and those produced by bacterial infection in the wild-type background. Analysis of the impact of the two atrboh mutations on these profiles provided further evidence that AtRbohF interacts closely with intracellular oxidative stress to tune dynamic metabolic responses during infection. Thus, AtRbohF appears to be a key player not only in HR-related cell death but also in regulating metabolomic responses and resistance. Based on the results obtained during the three types of interaction, a model is proposed of how NADPH oxidases and intracellular ROS interact to determine the outcome of pathogen defence responses.