Reciprocal Interaction of the Circadian Clock with the Iron Homeostasis Network in Arabidopsis

Reciprocal Interaction of the Circadian Clock with the Iron Homeostasis Network in Arabidopsis
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DOI:
10.1104/pp.112.208603
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发表时间:
2013-02-01
期刊:
影响因子:
7.4
通讯作者:
McClung, C. Robertson
McClung, C. Robertson
中科院分区:
生物学1区
文献类型:
--
作者:
Hong, Sunghyun;Kim, Sun A.;McClung, C. Robertson

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被引文献

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在植物中,铁(Fe)的吸收和稳态是生存的关键,这些过程在转录和转录后水平受到严格调控。生物钟是一种内源性振荡机制,允许生物体预测环境变化,以协调生物过程彼此之间以及与环境昼夜周期。植物生物钟通过转录本的节律性表达来控制许多生理过程。在这项研究中,我们研究了三个铁稳态基因(铁调节转运蛋白1 [IRT 1],碱性螺旋环螺旋39,铁蛋白1)在拟南芥(拟南芥)的表达启动子:荧光素酶转基因株系。这些启动子中的每一个都表现出转录的昼夜调节。生物钟监测多个时钟输出,并使用这些输出作为输入来调制时钟功能。我们表明,这也是真实的Fe状态。缺铁导致昼夜节律周期延长。我们询问了铁稳态反应受损的突变体,包括irt 1 -1,它缺乏主要的高亲和力铁转运蛋白,和fit-2,它缺乏铁缺乏诱导的转录因子1,一种基本的螺旋-环-螺旋转录因子诱导铁缺乏反应。这两种突变体表现出缺铁的症状,包括昼夜节律周期延长。为了确定哪些成分参与了昼夜节律和Fe稳态网络之间的这种串扰,我们测试了时钟或Fe稳态相关的突变体。在特定的时钟基因组件的突变体缺陷的周期长度的变化,在野生型中观察到的不同铁条件下,这表明这些突变体受损的铁稳态和昼夜节律钟之间的串扰。
In plants, iron (Fe) uptake and homeostasis are critical for survival, and these processes are tightly regulated at the transcriptional and posttranscriptional levels. Circadian clocks are endogenous oscillating mechanisms that allow an organism to anticipate environmental changes to coordinate biological processes both with one another and with the environmental day/night cycle. The plant circadian clock controls many physiological processes through rhythmic expression of transcripts. In this study, we examined the expression of three Fe homeostasis genes (IRON REGULATED TRANSPORTER1 [IRT1], BASIC HELIX LOOP HELIX39, and FERRITIN1) in Arabidopsis (Arabidopsis thaliana) using promoter: LUCIFERASE transgenic lines. Each of these promoters showed circadian regulation of transcription. The circadian clock monitors a number of clock outputs and uses these outputs as inputs to modulate clock function. We show that this is also true for Fe status. Fe deficiency results in a lengthened circadian period. We interrogated mutants impaired in the Fe homeostasis response, including irt1-1, which lacks the major high-affinity Fe transporter, and fit-2, which lacks Fe deficiency-induced TRANSCRIPTION FACTOR1, a basic helix-loop-helix transcription factor necessary for induction of the Fe deficiency response. Both mutants exhibit symptoms of Fe deficiency, including lengthened circadian period. To determine which components are involved in this cross talk between the circadian and Fe homeostasis networks, we tested clock-or Fe homeostasis-related mutants. Mutants defective in specific clock gene components were resistant to the change in period length under different Fe conditions observed in the wild type, suggesting that these mutants are impaired in cross talk between Fe homeostasis and the circadian clock.