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FE UPTAKE-INDUCING PEPTIDE1 通过调控拟南芥血管组织中铁缺乏响应基因来维持铁的转运。

FE UPTAKE-INDUCING PEPTIDE1 maintains Fe translocation by controlling Fe deficiency response genes in the vascular tissue of Arabidopsis.

机构信息

Group of Environmental Stress Response Systems, Institute of Plant Science and Resources, Okayama University, Okayama, Japan.

Group of Plant Stress Physiology, Institute of Plant Science and Resources, Okayama University, Okayama, Japan.

出版信息

Plant Cell Environ. 2022 Nov;45(11):3322-3337. doi: 10.1111/pce.14424. Epub 2022 Sep 7.

DOI:10.1111/pce.14424
PMID:35993196
Abstract

FE UPTAKE-INDUCING PEPTIDE1 (FEP1), also named IRON MAN3 (IMA3) is a short peptide involved in the iron deficiency response in Arabidopsis thaliana. Recent studies uncovered its molecular function, but its physiological function in the systemic Fe response is not fully understood. To explore the physiological function of FEP1 in iron homoeostasis, we performed a transcriptome analysis using the FEP1 loss-of-function mutant fep1-1 and a transgenic line with oestrogen-inducible expression of FEP1. We determined that FEP1 specifically regulates several iron deficiency-responsive genes, indicating that FEP1 participates in iron translocation rather than iron uptake in roots. The iron concentration in xylem sap under iron-deficient conditions was lower in the fep1-1 mutant and higher in FEP1-induced transgenic plants compared with the wild type (WT). Perls staining revealed a greater accumulation of iron in the cortex of fep1-1 roots than in the WT root cortex, although total iron levels in roots were comparable in the two genotypes. Moreover, the fep1-1 mutation partially suppressed the iron overaccumulation phenotype in the leaves of the oligopeptide transporter3-2 (opt3-2) mutant. These data suggest that FEP1 plays a pivotal role in iron movement and in maintaining the iron quota in vascular tissues in Arabidopsis.

摘要

铁缺乏诱导肽 1(FEP1),也称为铁 3 号蛋白(IMA3),是拟南芥缺铁响应中涉及的短肽。最近的研究揭示了其分子功能,但它在系统性铁响应中的生理功能尚未完全理解。为了探索 FEP1 在铁稳态中的生理功能,我们使用 FEP1 功能丧失突变体 fep1-1 和具有雌激素诱导 FEP1 表达的转基因系进行了转录组分析。我们确定 FEP1 特异性调节几个缺铁响应基因,表明 FEP1 参与铁转运而不是根系中铁的摄取。与野生型(WT)相比,缺铁条件下木质部汁液中的铁浓度在 fep1-1 突变体中较低,在 FEP1 诱导的转基因植物中较高。Perls 染色显示 fep1-1 根皮层中的铁积累多于 WT 根皮层,尽管两种基因型的根中总铁水平相当。此外,fep1-1 突变部分抑制了寡肽转运体 3-2(opt3-2)突变体叶片中铁的过度积累表型。这些数据表明 FEP1 在拟南芥中铁的移动和维持血管组织中铁配额中起着关键作用。

相似文献

1
FE UPTAKE-INDUCING PEPTIDE1 maintains Fe translocation by controlling Fe deficiency response genes in the vascular tissue of Arabidopsis.FE UPTAKE-INDUCING PEPTIDE1 通过调控拟南芥血管组织中铁缺乏响应基因来维持铁的转运。
Plant Cell Environ. 2022 Nov;45(11):3322-3337. doi: 10.1111/pce.14424. Epub 2022 Sep 7.
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The Putative Peptide Gene FEP1 Regulates Iron Deficiency Response in Arabidopsis.假定肽基因 FEP1 调控拟南芥缺铁应答。
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Iron Availability within the Leaf Vasculature Determines the Magnitude of Iron Deficiency Responses in Source and Sink Tissues in Arabidopsis.叶维管束内的铁供应决定了拟南芥源库组织缺铁响应的程度。
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Changes in iron availability in Arabidopsis are rapidly sensed in the leaf vasculature and impaired sensing leads to opposite transcriptional programs in leaves and roots.拟南芥中铁供应的变化在叶片脉管系统中迅速被感知,而感知受损会导致叶片和根系中相反的转录程序。
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BRUTUS and its paralogs, BTS LIKE1 and BTS LIKE2, encode important negative regulators of the iron deficiency response in Arabidopsis thaliana.BRUTUS 及其同源物 BTS LIKE1 和 BTS LIKE2 编码拟南芥中铁缺乏反应的重要负调控因子。
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Loss of OPT3 function decreases phloem copper levels and impairs crosstalk between copper and iron homeostasis and shoot-to-root signaling in Arabidopsis thaliana.OPT3 功能丧失会降低韧皮部铜含量,并损害拟南芥中铜和铁稳态以及地上部到根部信号转导之间的串扰。
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Root-to-shoot iron partitioning in Arabidopsis requires IRON-REGULATED TRANSPORTER1 (IRT1) protein but not its iron(II) transport function.拟南芥的根到梢铁分配需要铁调节转运蛋白 1(IRT1)蛋白,但不需要其铁(II)转运功能。
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OPT3 is a component of the iron-signaling network between leaves and roots and misregulation of OPT3 leads to an over-accumulation of cadmium in seeds.OPT3是叶片与根系之间铁信号网络的一个组成部分,OPT3调控失常会导致种子中镉的过度积累。
Mol Plant. 2014 Sep;7(9):1455-1469. doi: 10.1093/mp/ssu067. Epub 2014 May 31.

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