| アイテムタイプ |
学術雑誌論文 / Journal Article(1) |
| 公開日 |
2025-07-31 |
| タイトル |
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タイトル |
Arabidopsis SDG proteins mediate Polycomb removal and transcription-coupled H3K36 methylation for gene activation |
| 言語 |
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言語 |
eng |
| 資源タイプ |
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資源タイプ |
journal article |
| アクセス権 |
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アクセス権 |
open access |
| 著者 |
Wang, Yicong
Abe, Masato
Kadoya, Yuka
Saiki, Takeru
Imai, Kanae
Wang, Xuejing
To, Taiko Kim
Inagaki, Soichi
Suzuki, Takamasa
Kakutani, Tetsuji
伊藤, 寿朗
山口, 暢俊
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| 抄録 |
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内容記述タイプ |
Abstract |
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内容記述 |
Polycomb Repressive Complex 2 (PRC2) recognizes Polycomb response elements (PREs) and catalyzes trimethylation of histone H3 on lysine 27 (H3K27me3) for gene silencing. This silencing is counteracted by H3K36 methylation for epigenetic activation of gene expression. Here, we show that the Arabidopsis thaliana H3K36 methyltransferases SET DOMAIN-CONTAINING PROTEIN 7 (SDG7) and SDG8 antagonize PRC2-mediated silencing and establish H3K36 methylation patterns with the general transcription machinery. The sdg7 sdg8 double mutant shows developmental defects and lower H3K36me2 and H3K36me3 levels. SDG7 preferentially binds near PREs, but SDG8 is recruited to H3K36 methylation peaks. The sdg7 sdg8 phenotypes are partially rescued by loss of Polycomb function. SDG7 overlaps with PRC2 and its recruiters on chromatin and evicts them from shared target genes when conditionally induced. SDG8 and RNA Polymerase II associate at SDG- and RNA POLYMERASE II ASSOCIATED FACTOR 1 complex-regulated targets for H3K36 methylation and transcription. These results suggest that SDG proteins evict PRC2 from PREs to prevent H3K27me3 deposition and activate target genes via transcription-coupled H3K36 methylation. Post-translational modifications of histone proteins play critical roles in regulating the physical properties of chromatin and defining the transcriptional state1. Among various histone modifications, histone methylation primarily occurs on lysine or arginine residues and can affect both chromatin condensation and transcriptional states. Trimethylation of lysine 27 on histone H3 (H3K27me3) is associated with downregulation of nearby genes, leading to the formation of heterochromatic regions that are responsive to certain conditions2. Methylation of lysine 4 and 36 on histone H3 (H3K4 and H3K36) is present on nucleosomes of transcriptionally active chromatin2. Histone modifications are complex and reflect the topological constraints caused by nearby modifications. Indeed, the presence of particular histone modifications can promote the addition of the same type of modification or the removal of different types: for example, higher H3K36 levels hinder H3K27me3 deposition3. Such interconnected epigenetic systems, characterized by bistable states, determine the transcriptional activity of each gene. Methylation marks can be added to histones by specific enzymes called methyltransferases. In all eukaryotic organisms, the activity of H3K27 methyltransferase is controlled by Polycomb Repressive Complex 2 (PRC2)4$20136. In Drosophila melanogaster, PRC2 contains four core subunits, including Enhancer of zeste [E(z)] with a catalytic SET domain and Extra sex comb (Esc)6. Arabidopsis (Arabidopsis thaliana) has three E(z) methyltransferases homologous to E(z)$2014CURLY LEAF (CLF), SWINGER (SWN) and MEDEA (MEA)$2014that catalyze H3K27me37. Because these methyltransferases act redundantly, higher-order mutants exhibit more severe developmental defects than any single mutant8. Arabidopsis FERTILIZATION INDEPENDENT ENDOSPERM (FIE) is a WD40 homolog of D. melanogaster Esc. PRC2 interacts with multiple transcription factors through its subunits and is recruited to cis-regulatory regions of several hundred base pairs in length called Polycomb Response Elements (PREs). Proper PRC2 placement by trans-acting factors, such as BASIC PENTACYSTEINE (BPC), APETALA2 (AP2)-like or C2H2 zinc-finger (ZnF) family members, triggers the initial deposition of H3K27me39,10. The opposing H3K36 trimethylation is regulated by SET DOMAIN GROUP8 (SDG8)11. SDG8 interacts with the transcription machinery, namely RNA polymerase II (RNA Pol II) and the polymerase-associated factor 1 (Paf1) complex (PAF1C)12. PAF1C components include VERNALIZATION INDEPENDENCE2 (VIP2, also named EARLY FLOWERING 7 [ELF7]), VIP3, VIP4, VIP5 and VIP6 (also named ELF8)13. Despite the critical importance of H3K36me3 and the general transcription machinery, sdg8 single mutants show relatively weak developmental defects14, suggesting that the full function of SDG8 may be masked by partial redundancy with closely related protein(s). However, the identity of such factor(s) and their roles in the epigenetic systems have not been established. In this study, we focus on one SDG8 homolog, SDG7, to consolidate the existing knowledge of the epigenetic interaction network along with the general transcription machinery. We show that the sdg7 sdg8 double mutant exhibits developmental abnormalities and a notable decrease in both H3K36me2 and H3K36me3 levels, supporting the partial redundancy of SDG7 and SDG8. We also examine the genomic regions to which SDG7 and SDG8 are recruited and explore the connection between the sdg7 sdg8 mutant phenotypes, the PRC2 complex, and RNA Pol II. We propose that SDGs displace PRC2 from PREs, preventing the deposition of H3K27me3 and activating the expression of target genes through transcription-coupled H3K36 methylation. |
| 書誌情報 |
en : eLife
ページ数 32,
発行日 2024-09-10
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| 出版者 |
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出版者 |
eLife Sciences Publications |
| ISSN |
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収録物識別子タイプ |
EISSN |
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収録物識別子 |
2050-084X |
| 出版者版DOI |
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関連タイプ |
isReplacedBy |
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識別子タイプ |
DOI |
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関連識別子 |
https://doi.org/10.7554/eLife.100905.1 |
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関連タイプ |
isReplacedBy |
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識別子タイプ |
URI |
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関連識別子 |
https://elifesciences.org/reviewed-preprints/100905v1 |
| 権利 |
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権利情報Resource |
https://creativecommons.org/licenses/by/4.0/ |
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権利情報 |
$00A9 2024, Wang et al. This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited. |
| 著者版フラグ |
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出版タイプ |
NA |
| 助成情報 |
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助成機関名 |
Japan Society for the Promotion of Science (JSPS) |
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研究課題番号 |
23H02503 |
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研究課題番号URI |
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23K27195/ |
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研究課題名 |
花弁基部の細胞動態に注目した脱離制御機構の解明 |
| 助成情報 |
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助成機関名 |
Japan Society for the Promotion of Science (JSPS) |
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研究課題番号 |
19K22431 |
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研究課題番号URI |
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-19K22431/ |
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研究課題名 |
フィールド条件で植物の高温順化を制御するゲノム・エピゲノムの機能解析 |
| 助成情報 |
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助成機関名 |
Japan Society for the Promotion of Science (JSPS) |
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研究課題番号 |
21H05663 |
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研究課題番号URI |
https://kaken.nii.ac.jp/grant/KAKENHI-PUBLICLY-21H05663/ |
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研究課題名 |
不規則な温度に対する植物の多層的レジリエンス機構 |
| 助成情報 |
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助成機関名 |
Japan Society for the Promotion of Science (JSPS) |
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研究課題番号 |
23H04968 |
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研究課題番号URI |
https://kaken.nii.ac.jp/grant/KAKENHI-PLANNED-23H04968/ |
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研究課題名 |
BVOC放出とストレス耐性を連動させるエピゲノム分子基盤の解明 |
| 助成情報 |
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助成機関名 |
Daiichi Sankyo Foundation of Life Science |
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助成機関名 |
LOTTE Foundation |
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助成機関名 |
Ohsumi Frontier Science Foundation |
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助成機関名 |
Japan Society for the Promotion of Science (JSPS) |
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研究課題番号 |
22K06180 |
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研究課題番号URI |
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-22K06180/ |
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研究課題名 |
エピゲノムパターン構築に不可欠な遺伝子と有害配列の識別メカニズムの解明 |
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助成機関名 |
Japan Society for the Promotion of Science (JSPS) |
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研究課題番号 |
21K19266 |
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研究課題番号URI |
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-21K19266/ |
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研究課題名 |
近縁種交配体ゲノムによる植物個体死の定義および制御系の理解 |
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助成機関名 |
Japan Society for the Promotion of Science (JSPS) |
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研究課題番号 |
20H00470 |
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研究課題番号URI |
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-20H00470/ |
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研究課題名 |
植物幹細胞の増殖・分化・老化のバランスによる花の数とサイズの制御機構 |
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助成機関名 |
Japan Society for the Promotion of Science (JSPS) |
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研究課題番号 |
22H05176 |
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研究課題番号URI |
https://kaken.nii.ac.jp/grant/KAKENHI-PLANNED-22H05176/ |
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研究課題名 |
両性花における動物を利用した他殖促進機構の構築原理 |
