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本文引用的文献

1
FIT, a regulatory hub for iron deficiency and stress signaling in roots, and FIT-dependent and -independent gene signatures.FIT,根中缺铁和应激信号的调控枢纽,以及依赖和不依赖 FIT 的基因特征。
J Exp Bot. 2020 Mar 12;71(5):1694-1705. doi: 10.1093/jxb/eraa012.
2
The iron deficiency response in requires the phosphorylated transcription factor URI.需要磷酸化转录因子 URI 来响应中的铁缺乏。
Proc Natl Acad Sci U S A. 2019 Dec 10;116(50):24933-24942. doi: 10.1073/pnas.1916892116. Epub 2019 Nov 27.
3
The Transcription Factor bHLH121 Interacts with bHLH105 (ILR3) and Its Closest Homologs to Regulate Iron Homeostasis in Arabidopsis.转录因子 bHLH121 与 bHLH105(ILR3)及其最接近的同源物相互作用,以调节拟南芥中的铁稳态。
Plant Cell. 2020 Feb;32(2):508-524. doi: 10.1105/tpc.19.00541. Epub 2019 Nov 27.
4
PRC2-Mediated H3K27me3 Contributes to Transcriptional Regulation of FIT-Dependent Iron Deficiency Response.PRC2介导的H3K27me3参与FIT依赖的缺铁反应的转录调控。
Front Plant Sci. 2019 May 16;10:627. doi: 10.3389/fpls.2019.00627. eCollection 2019.
5
The bifunctional transporter-receptor IRT1 at the heart of metal sensing and signalling.IRT1 是一种多功能转运体-受体,位于金属感应和信号转导的核心。
New Phytol. 2019 Aug;223(3):1173-1178. doi: 10.1111/nph.15826. Epub 2019 Apr 24.
6
Understanding the Complexity of Iron Sensing and Signaling Cascades in Plants.理解植物中铁感应和信号级联的复杂性。
Plant Cell Physiol. 2019 Jul 1;60(7):1440-1446. doi: 10.1093/pcp/pcz038.
7
Transcriptional integration of the responses to iron availability in Arabidopsis by the bHLH factor ILR3.拟南芥 bHLH 因子 ILR3 对铁可用性响应的转录整合。
New Phytol. 2019 Aug;223(3):1433-1446. doi: 10.1111/nph.15753. Epub 2019 Mar 25.
8
The Transcriptional Control of Iron Homeostasis in Plants: A Tale of bHLH Transcription Factors?植物中铁稳态的转录调控:bHLH转录因子的故事?
Front Plant Sci. 2019 Jan 18;10:6. doi: 10.3389/fpls.2019.00006. eCollection 2019.
9
CIPK11-Dependent Phosphorylation Modulates FIT Activity to Promote Arabidopsis Iron Acquisition in Response to Calcium Signaling.CIPK11 依赖性磷酸化调节 FIT 活性以响应钙信号促进拟南芥铁的获取。
Dev Cell. 2019 Mar 11;48(5):726-740.e10. doi: 10.1016/j.devcel.2019.01.006. Epub 2019 Jan 31.
10
Iron is a centrally bound cofactor of specifier proteins involved in glucosinolate breakdown.铁是参与硫代葡萄糖苷分解的特异性蛋白的中心结合辅因子。
PLoS One. 2018 Nov 5;13(11):e0205755. doi: 10.1371/journal.pone.0205755. eCollection 2018.

PRC2 介导的 H3K27me3 调控. 中的 shoot 铁稳态。

PRC2-mediated H3K27me3 modulates shoot iron homeostasis in .

机构信息

Department of Biology, Amherst College , Amherst, MA, USA.

出版信息

Plant Signal Behav. 2020 Sep 1;15(9):1784549. doi: 10.1080/15592324.2020.1784549. Epub 2020 Jun 27.

DOI:10.1080/15592324.2020.1784549
PMID:32594838
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8550290/
Abstract

Plants use intricate mechanisms to adapt to changing iron conditions because iron is essential and also one of the most limiting nutrients for plant growth. Furthermore, iron is potentially toxic in excess and must be tightly regulated. Previously, we showed that chromatin remodeling via histone 3 lysine 27 trimethylation (H3K27me3) modulates the expression of FIT-dependent genes under iron deficiency in roots. This study builds on our previous findings, showing that H3K27me3 also modulates iron regulation in shoots. In the mutant, which lacks the predominant H3K27 tri-methyltransferase, we detected increased iron translocation to shoots under iron deficiency as compared to wild type. Transcriptomic analysis of shoots also revealed differential expression of genes consistent with higher iron levels in shoots than wild type shoots under iron-deficient conditions. In addition, we verify that and , two genes involved in signaling iron status from shoots to roots, are direct targets of H3K27me3 and reveal iron-dependent deposition of H3K27me3 on these loci. This study contributes to a better understanding of the molecular mechanisms behind iron regulation in plants, as the effect of PRC2-mediated H3K27me3 on iron homeostasis genes expressed in the shoots has not been previously reported to our knowledge.

摘要

植物利用复杂的机制来适应不断变化的铁条件,因为铁是必需的,也是限制植物生长的最重要营养物质之一。此外,过量的铁具有潜在毒性,必须进行严格的调节。先前,我们表明通过组蛋白 3 赖氨酸 27 三甲基化(H3K27me3)的染色质重塑调节根中缺铁条件下 FIT 依赖性基因的表达。本研究建立在我们之前的发现之上,表明 H3K27me3 也调节了叶片中的铁调节。在缺乏主要 H3K27 三甲基转移酶的 突变体中,与野生型相比,我们检测到缺铁条件下铁向叶片的转运增加。叶片的转录组分析还揭示了与缺铁条件下 叶片中比野生型叶片中更高铁水平一致的基因的差异表达。此外,我们验证了 和 ,这两个基因涉及从叶片向根系传递铁状态的信号,是 H3K27me3 的直接靶标,并揭示了这些基因座上铁依赖性 H3K27me3 的沉积。本研究有助于更好地理解植物中铁调节背后的分子机制,因为我们所知,以前没有报道过 PRC2 介导的 H3K27me3 对在叶片中表达的铁稳态基因的影响。