A Matrix Protein Silences Transposons and Repeats through Interaction with Retinoblastoma-Associated Proteins
Epigenetic regulation helps to maintain genomic integrity by suppressing transposable elements (TEs) and also controls key developmental processes, such as flowering time [1–3]. To prevent TEs from causing rearrangements and mutations, TE and TE-like repetitive DNA sequences are usually methylated,...
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Published in | Current biology Vol. 23; no. 4; pp. 345 - 350 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
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Elsevier Inc
18.02.2013
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Abstract | Epigenetic regulation helps to maintain genomic integrity by suppressing transposable elements (TEs) and also controls key developmental processes, such as flowering time [1–3]. To prevent TEs from causing rearrangements and mutations, TE and TE-like repetitive DNA sequences are usually methylated, whereas histones are hypoacetylated and methylated on specific residues (e.g., H3 lysine 9 dimethylation [H3K9me2]) [4, 5]. TEs and repeats can also attenuate gene expression [2, 6–8]. However, how various histone modifiers are recruited to target loci is not well understood. Here we show that knockdown of the nuclear matrix protein with AT-hook DNA binding motifs [9–11] TRANSPOSABLE ELEMENT SILENCING VIA AT-HOOK (TEK) in Arabidopsis Landsberg erecta results in robust activation of various TEs, the TE-like repeat-containing floral repressor genes FLOWERING LOCUS C (FLC) and FWA [1, 2, 12]. This derepression is associated with chromatin conformational changes, increased histone acetylation, reduced H3K9me2, and even TE transposition. TEK directly binds to an FLC-repressive regulatory region and the silencing repeats of FWA and associates with Arabidopsis homologs of the Retinoblastoma-associated protein 46/48, FVE and MSI5, which mediate histone deacetylation [13, 14]. We propose that the nuclear matrix protein TEK acts in the maintenance of genome integrity by silencing TE and repeat-containing genes.
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► The Arabidopsis matrix protein TEK silences transposons and repeat-containing genes ► Binding of TEK on targets affects chromatin conformation and histone modifications ► TEK protein associates with FVE/MSI5-containing histone deacetylation complex ► TEK directs repressive modification as a key structural component in gene silencing |
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AbstractList | Epigenetic regulation helps to maintain genomic integrity by suppressing transposable elements (TEs) and also controls key developmental processes, such as flowering time. To prevent TEs from causing rearrangements and mutations, TE and TE-like repetitive DNA sequences are usually methylated, whereas histones are hypoacetylated and methylated on specific residues (e.g., H3 lysine 9 dimethylation [H3K9me2]). TEs and repeats can also attenuate gene expression. However, how various histone modifiers are recruited to target loci is not well understood. Here we show that knockdown of the nuclear matrix protein with AT-hook DNA binding motifs TRANSPOSABLE ELEMENT SILENCING VIA AT-HOOK (TEK) in Arabidopsis Landsberg erecta results in robust activation of various TEs, the TE-like repeat-containing floral repressor genes FLOWERING LOCUS C (FLC) and FWA. This derepression is associated with chromatin conformational changes, increased histone acetylation, reduced H3K9me2, and even TE transposition. TEK directly binds to an FLC-repressive regulatory region and the silencing repeats of FWA and associates with Arabidopsis homologs of the Retinoblastoma-associated protein 46/48, FVE and MSI5, which mediate histone deacetylation. We propose that the nuclear matrix protein TEK acts in the maintenance of genome integrity by silencing TE and repeat-containing genes. Epigenetic regulation helps to maintain genomic integrity by suppressing transposable elements (TEs) and also controls key developmental processes, such as flowering time [1-3]. To prevent TEs from causing rearrangements and mutations, TE and TE-like repetitive DNA sequences are usually methylated, whereas histones are hypoacetylated and methylated on specific residues (e.g., H3 lysine 9 dimethylation [H3K9me2]) [4, 5]. TEs and repeats can also attenuate gene expression [2, 6-8]. However, how various histone modifiers are recruited to target loci is not well understood. Here we show that knockdown of the nuclear matrix protein with AT-hook DNA binding motifs [9-11] TRANSPOSABLE ELEMENT SILENCING VIA AT-HOOK (TEK) in Arabidopsis Landsberg erecta results in robust activation of various TEs, the TE-like repeat-containing floral repressor genes FLOWERING LOCUS C (FLC) and FWA [1, 2, 12]. This derepression is associated with chromatin conformational changes, increased histone acetylation, reduced H3K9me2, and even TE transposition. TEK directly binds to an FLC-repressive regulatory region and the silencing repeats of FWA and associates with Arabidopsis homologs of the Retinoblastoma-associated protein 46/48, FVE and MSI5, which mediate histone deacetylation [13, 14]. We propose that the nuclear matrix protein TEK acts in the maintenance of genome integrity by silencing TE and repeat-containing genes. Epigenetic regulation helps to maintain genomic integrity by suppressing transposable elements (TEs) and also controls key developmental processes, such as flowering time [1–3]. To prevent TEs from causing rearrangements and mutations, TE and TE-like repetitive DNA sequences are usually methylated, whereas histones are hypoacetylated and methylated on specific residues (e.g., H3 lysine 9 dimethylation [H3K9me2]) [4, 5]. TEs and repeats can also attenuate gene expression [2, 6–8]. However, how various histone modifiers are recruited to target loci is not well understood. Here we show that knockdown of the nuclear matrix protein with AT-hook DNA binding motifs [9–11] TRANSPOSABLE ELEMENT SILENCING VIA AT-HOOK (TEK) in Arabidopsis Landsberg erecta results in robust activation of various TEs, the TE-like repeat-containing floral repressor genes FLOWERING LOCUS C (FLC) and FWA [1, 2, 12]. This derepression is associated with chromatin conformational changes, increased histone acetylation, reduced H3K9me2, and even TE transposition. TEK directly binds to an FLC-repressive regulatory region and the silencing repeats of FWA and associates with Arabidopsis homologs of the Retinoblastoma-associated protein 46/48, FVE and MSI5, which mediate histone deacetylation [13, 14]. We propose that the nuclear matrix protein TEK acts in the maintenance of genome integrity by silencing TE and repeat-containing genes. [Display omitted] ► The Arabidopsis matrix protein TEK silences transposons and repeat-containing genes ► Binding of TEK on targets affects chromatin conformation and histone modifications ► TEK protein associates with FVE/MSI5-containing histone deacetylation complex ► TEK directs repressive modification as a key structural component in gene silencing |
Author | Wang, Yizhong Sun, Bo Gu, Xiaofeng He, Yuehui Gan, Eng-Seng Ito, Toshiro Stroud, Hume Jacobsen, Steven E. Ng, Kian-Hong Xu, Yifeng |
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SubjectTerms | acetylation Arabidopsis Arabidopsis - genetics Chromatin Chromatin - genetics Chromatin - metabolism Deacetylation Derepression DNA Methylation DNA Transposable Elements - genetics DNA-binding domains DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Epigenesis, Genetic epigenetics Flowering Gene expression Gene Expression Regulation, Plant genes Genomes genomics Histones loci Lysine matrix protein Methylation Mutation nuclear matrix Nuclear Matrix-Associated Proteins - genetics Regulatory sequences Repeated DNA sequences Repressors Retinoblastoma Binding Proteins - metabolism retinoblastoma-associated protein RNA Interference RNA, Small Interfering Transposition Transposons |
Title | A Matrix Protein Silences Transposons and Repeats through Interaction with Retinoblastoma-Associated Proteins |
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