ZINC FINGER OF ARABIDOPSIS THALIANA12 (ZAT12) Interacts with FER-LIKE IRON DEFICIENCY- INDUCED TRANSCRIPTION FACTOR (FIT) Linking Iron Deficiency and Oxidative Stress Responses
ZINC FINGER OF ARABIDOPSIS THALIANA12 (ZAT12) Interacts with FER-LIKE IRON DEFICIENCY- INDUCED TRANSCRIPTION FACTOR (FIT) Linking Iron Deficiency and Oxidative Stress Responses
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DOI：
10.1104/pp.15.01589
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发表时间：
2016-01-01
期刊：
影响因子：
7.4
通讯作者：
Bauer, Petra
中科院分区：
文献类型：
--
作者：
Cham Thi Tuyet Le;Brumbarova, Tzvetina;Bauer, Petra
在缺铁条件下生长的植物诱导出一组提高根系吸收铁效率的基因。在拟南芥（Arabidopsis thaliana）中，这种反应的中心调节因子是基本的螺旋-环-螺旋转录因子FERLIKE铁缺乏诱导转录因子（FIT）。FIT活性受蛋白质相互作用的调节，蛋白质相互作用也用于整合刺激和可能抑制铁摄取的外部信号。在寻找调节FIT功能的信号元件的过程中，我们发现了拟南芥12 （ZAT12）的锌指，这是一种非生物应激诱导的转录因子。ZAT12与FIT相互作用，依赖于乙烯响应元件结合因子相关的两亲性抑制基序的存在。ZAT12蛋白在根早分化区表达，其丰度受根层特异性调控。在缺乏ZAT12的情况下，FIT表达上调，表明ZAT12对铁摄取有负面影响。与此一致的是，在铁充足的情况下，zat12功能丧失突变体的铁含量高于野生型。我们发现，在缺铁的情况下，过氧化氢（H2O2）水平以fit依赖的方式增强。反过来，FIT蛋白被H2O2稳定，但只有在ZAT12存在的情况下，这表明H2O2是铁缺乏反应的信号。我们提出氧化应激诱导的ZAT12作为铁获取的负调节因子。H2O2介导植物对长时间胁迫反应负调控的模型可能适用于多种胁迫条件。
Plants grown under iron (Fe)-deficient conditions induce a set of genes that enhance the efficiency of Fe uptake by the roots. In Arabidopsis (Arabidopsis thaliana), the central regulator of this response is the basic helix-loop-helix transcription factor FERLIKE IRON DEFICIENCY-INDUCED TRANSCRIPTION FACTOR (FIT). FIT activity is regulated by protein-protein interactions, which also serve to integrate external signals that stimulate and possibly inhibit Fe uptake. In the search of signaling components regulating FIT function, we identified ZINC FINGER OF ARABIDOPSIS THALIANA12 (ZAT12), an abiotic stress-induced transcription factor. ZAT12 interacted with FIT, dependent on the presence of the ethylene-responsive element-binding factor-associated amphiphilic repression motif. ZAT12 protein was found expressed in the root early differentiation zone, where its abundance was modulated in a root layer-specific manner. In the absence of ZAT12, FIT expression was upregulated, suggesting a negative effect of ZAT12 on Fe uptake. Consistently, zat12 loss-of-function mutants had higher Fe content than the wild type at sufficient Fe. We found that under Fe deficiency, hydrogen peroxide (H2O2) levels were enhanced in a FIT-dependent manner. FIT protein, in turn, was stabilized by H2O2 but only in the presence of ZAT12, showing that H2O2 serves as a signal for Fe deficiency responses. We propose that oxidative stress-induced ZAT12 functions as a negative regulator of Fe acquisition. A model where H2O2 mediates the negative regulation of plant responses to prolonged stress might be applicable to a variety of stress conditions.