Arabidopsis TRB proteins function in H3K4me3 demethylation by recruiting the JMJ14 complex
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ABSTRACT:
ORGANISM(S): Arabidopsis thaliana
PROVIDER: GSE204681 | GEO | 2023/02/12
REPOSITORIES: GEO
Similar Datasets
Project description:Arabidopsis telomeric repeat binding factors (TRBs) can bind telomeric DNA sequences to protect telomeres from degradation. TRBs can also recruit Polycomb Repressive Complex 2 (PRC2) to deposit tri-methylation of H3 lysine 27 (H3K27me3) over certain target loci. Here, we demonstrate that TRBs also associate and colocalize with JUMONJI14 (JMJ14) and trigger H3K4me3 demethylation at some loci. The trb1/2/3 triple mutant and the jmj14-1 mutant show an increased level of H3K4me3 over TRB and JMJ14 binding sites, resulting in up-regulation of their target genes. Furthermore, tethering TRBs to the promoter region of genes with an artificial zinc finger (TRB-ZF) successfully triggers target gene silencing, as well as H3K27me3 deposition, and H3K4me3 removal. Interestingly, JMJ14 is predominantly recruited to ZF off-target sites with low levels of H3K4me3, which is accompanied with TRB-ZFs triggered H3K4me3 removal at these loci. These results suggest that TRB proteins coordinate PRC2 and JMJ14 activities to repress target genes via H3K27me3 deposition and H3K4me3 removal.
2023-02-22 | MSV000091349 | MassIVE
Project description:TELOMERE REPEAT BINDING proteins (TRBs) are plant specific transcriptional regulators that combine two DNA binding domains: the GH1 domain shared with H1 linker histones and the Myb/SANT domain that specifically recognize AAACCCT, the telomeric motif, present at telomeres, centromere-proximal Interstitial Telomeric Repeats (ITRs) and at promoters of numerous protein-coding genes. TRB1, TRB2 and TRB3 (TRB1-3) proteins collaborate with PRC2 and JMJ14 for deposition of H3K27me3 and removal of H3K4me3 to induce transcriptional repression in a functionally redundant manner. Here we report that TRB4 and TRB5, which belong to a separate TRB clade conserved among spermatophytes, fulfill chromatin roles distinct from TRB1-3. We show that TRB4 and TRB5 are involved in the transcriptional control of several hundred genes involved in developmental responses to environmental cues and in consequence TRB4 and TRB5 loss of function plants present developmental growth defects including delayed flowering. Most of the trb4 trb5 transcriptomic defects differ from those of trb1 trb2 trb3, suggesting a distinct mode of action at the chromatin level. Indeed, TRB4 binds to several thousand sites in the genome, mainly to TSS and promoter regions of transcriptionally active and H3K4me3-marked genes, but it does not affect global H3K4me3 levels. In contrast to TRB1-3, TRB4 is not enriched at H3K27me3-marked gene bodies, and combined loss of TRB4 and TRB5 affects H3K27me3 only at a small subset of genes. Yet, TRB4 physically interacts with the catalytically active subunit of somatic PRC2 complexes CURLY LEAF (CLF). Unexpectedly, loss of TRB4 and TRB5 partially suppresses developmental defects of clf mutant plants, likely through their role as positive transcriptional regulators of the key flowering genes SOC1 and FT. We further show that TRB4 and TRB1 share multiple target genes and reveal physical and genetic interactions between TRBs of the two distinct clades, altogether unveiling that TRB proteins engage in both positive and negative interplay with other members of the family to regulate plant development through PRC2-dependent and independent mechanisms.
2024-02-12 | GSE237185 | GEO
Project description:TELOMERE REPEAT BINDING proteins (TRBs) are plant specific transcriptional regulators that combine two DNA binding domains: the GH1 domain shared with H1 linker histones and the Myb/SANT domain that specifically recognize AAACCCT, the telomeric motif, present at telomeres, centromere-proximal Interstitial Telomeric Repeats (ITRs) and at promoters of numerous protein-coding genes. TRB1, TRB2 and TRB3 (TRB1-3) proteins collaborate with PRC2 and JMJ14 for deposition of H3K27me3 and removal of H3K4me3 to induce transcriptional repression in a functionally redundant manner. Here we report that TRB4 and TRB5, which belong to a separate TRB clade conserved among spermatophytes, fulfill chromatin roles distinct from TRB1-3. We show that TRB4 and TRB5 are involved in the transcriptional control of several hundred genes involved in developmental responses to environmental cues and in consequence TRB4 and TRB5 loss of function plants present developmental growth defects including delayed flowering. Most of the trb4 trb5 transcriptomic defects differ from those of trb1 trb2 trb3, suggesting a distinct mode of action at the chromatin level. Indeed, TRB4 binds to several thousand sites in the genome, mainly to TSS and promoter regions of transcriptionally active and H3K4me3-marked genes, but it does not affect global H3K4me3 levels. In contrast to TRB1-3, TRB4 is not enriched at H3K27me3-marked gene bodies, and combined loss of TRB4 and TRB5 affects H3K27me3 only at a small subset of genes. Yet, TRB4 physically interacts with the catalytically active subunit of somatic PRC2 complexes CURLY LEAF (CLF). Unexpectedly, loss of TRB4 and TRB5 partially suppresses developmental defects of clf mutant plants, likely through their role as positive transcriptional regulators of the key flowering genes SOC1 and FT. We further show that TRB4 and TRB1 share multiple target genes and reveal physical and genetic interactions between TRBs of the two distinct clades, altogether unveiling that TRB proteins engage in both positive and negative interplay with other members of the family to regulate plant development through PRC2-dependent and independent mechanisms.
2024-02-12 | GSE237158 | GEO
Project description:TELOMERE REPEAT BINDING proteins (TRBs) are plant specific transcriptional regulators that combine two DNA binding domains: the GH1 domain shared with H1 linker histones and the Myb/SANT domain that specifically recognize AAACCCT, the telomeric motif, present at telomeres, centromere-proximal Interstitial Telomeric Repeats (ITRs) and at promoters of numerous protein-coding genes. TRB1, TRB2 and TRB3 (TRB1-3) proteins collaborate with PRC2 and JMJ14 for deposition of H3K27me3 and removal of H3K4me3 to induce transcriptional repression in a functionally redundant manner. Here we report that TRB4 and TRB5, which belong to a separate TRB clade conserved among spermatophytes, fulfill chromatin roles distinct from TRB1-3. We show that TRB4 and TRB5 are involved in the transcriptional control of several hundred genes involved in developmental responses to environmental cues and in consequence TRB4 and TRB5 loss of function plants present developmental growth defects including delayed flowering. Most of the trb4 trb5 transcriptomic defects differ from those of trb1 trb2 trb3, suggesting a distinct mode of action at the chromatin level. Indeed, TRB4 binds to several thousand sites in the genome, mainly to TSS and promoter regions of transcriptionally active and H3K4me3-marked genes, but it does not affect global H3K4me3 levels. In contrast to TRB1-3, TRB4 is not enriched at H3K27me3-marked gene bodies, and combined loss of TRB4 and TRB5 affects H3K27me3 only at a small subset of genes. Yet, TRB4 physically interacts with the catalytically active subunit of somatic PRC2 complexes CURLY LEAF (CLF). Unexpectedly, loss of TRB4 and TRB5 partially suppresses developmental defects of clf mutant plants, likely through their role as positive transcriptional regulators of the key flowering genes SOC1 and FT. We further show that TRB4 and TRB1 share multiple target genes and reveal physical and genetic interactions between TRBs of the two distinct clades, altogether unveiling that TRB proteins engage in both positive and negative interplay with other members of the family to regulate plant development through PRC2-dependent and independent mechanisms.
2024-02-12 | GSE236267 | GEO
Project description:TELOMERE REPEAT BINDING proteins (TRBs) are plant specific transcriptional regulators that combine two DNA binding domains: the GH1 domain shared with H1 linker histones and the Myb/SANT domain that specifically recognize AAACCCT, the telomeric motif, present at telomeres, centromere-proximal Interstitial Telomeric Repeats (ITRs) and at promoters of numerous protein-coding genes. TRB1, TRB2 and TRB3 (TRB1-3) proteins collaborate with PRC2 and JMJ14 for deposition of H3K27me3 and removal of H3K4me3 to induce transcriptional repression in a functionally redundant manner. Here we report that TRB4 and TRB5, which belong to a separate TRB clade conserved among spermatophytes, fulfill chromatin roles distinct from TRB1-3. We show that TRB4 and TRB5 are involved in the transcriptional control of several hundred genes involved in developmental responses to environmental cues and in consequence TRB4 and TRB5 loss of function plants present developmental growth defects including delayed flowering. Most of the trb4 trb5 transcriptomic defects differ from those of trb1 trb2 trb3, suggesting a distinct mode of action at the chromatin level. Indeed, TRB4 binds to several thousand sites in the genome, mainly to TSS and promoter regions of transcriptionally active and H3K4me3-marked genes, but it does not affect global H3K4me3 levels. In contrast to TRB1-3, TRB4 is not enriched at H3K27me3-marked gene bodies, and combined loss of TRB4 and TRB5 affects H3K27me3 only at a small subset of genes. Yet, TRB4 physically interacts with the catalytically active subunit of somatic PRC2 complexes CURLY LEAF (CLF). Unexpectedly, loss of TRB4 and TRB5 partially suppresses developmental defects of clf mutant plants, likely through their role as positive transcriptional regulators of the key flowering genes SOC1 and FT. We further show that TRB4 and TRB1 share multiple target genes and reveal physical and genetic interactions between TRBs of the two distinct clades, altogether unveiling that TRB proteins engage in both positive and negative interplay with other members of the family to regulate plant development through PRC2-dependent and independent mechanisms.
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Project description:Chromatin architecture relies on histone H1 whose central globular domain (GH1) sits on the nucleosome dyad and carboxy-terminal domain associates with linker DNA. We report that Arabidopsis H1 positively influences H3K27me3 chromatin enrichment over protein-coding genes but oppositely prevents its accumulation on telomeres and heterochromatic Interstitial Telomeric Repeats (ITRs). Contrasting with their neighboring heterochromatic environment, pericentromeric ITR regions remain highly compacted and are more prone to long-distance interactions with telomeres in H1 mutant plants. The switch from H1-rich to H3K27me3-rich ITR chromatin is further accompanied by an invasion of GH1-Myb Telomeric Repeat Binding protein 1 (TRB1), a structural component of telomeres capable to trigger H3K27me3 deposition over protein-coding genes displaying short telomeric motifs. This dual effect led us to propose a competition mechanism between H1 and TRB that prevents massive H3K27me3 deposition over large blocks of repeated motifs, thereby contributing to regulate H3K27me3 homeostasis over the genome.
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Project description:Chromatin architecture relies on histone H1 whose central globular domain (GH1) sits on the nucleosome dyad and carboxy-terminal domain associates with linker DNA. We report that Arabidopsis H1 positively influences H3K27me3 chromatin enrichment over protein-coding genes but oppositely prevents its accumulation on telomeres and heterochromatic Interstitial Telomeric Repeats (ITRs). Contrasting with their neighboring heterochromatic environment, pericentromeric ITR regions remain highly compacted and are more prone to long-distance interactions with telomeres in H1 mutant plants. The switch from H1-rich to H3K27me3-rich ITR chromatin is further accompanied by an invasion of GH1-Myb Telomeric Repeat Binding protein 1 (TRB1), a structural component of telomeres capable to trigger H3K27me3 deposition over protein-coding genes displaying short telomeric motifs. This dual effect led us to propose a competition mechanism between H1 and TRB that prevents massive H3K27me3 deposition over large blocks of repeated motifs, thereby contributing to regulate H3K27me3 homeostasis over the genome.
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Project description:Chromatin architecture relies on histone H1 whose central globular domain (GH1) sits on the nucleosome dyad and carboxy-terminal domain associates with linker DNA. We report that Arabidopsis H1 positively influences H3K27me3 chromatin enrichment over protein-coding genes but oppositely prevents its accumulation on telomeres and heterochromatic Interstitial Telomeric Repeats (ITRs). Contrasting with their neighboring heterochromatic environment, pericentromeric ITR regions remain highly compacted and are more prone to long-distance interactions with telomeres in H1 mutant plants. The switch from H1-rich to H3K27me3-rich ITR chromatin is further accompanied by an invasion of GH1-Myb Telomeric Repeat Binding protein 1 (TRB1), a structural component of telomeres capable to trigger H3K27me3 deposition over protein-coding genes displaying short telomeric motifs. This dual effect led us to propose a competition mechanism between H1 and TRB that prevents massive H3K27me3 deposition over large blocks of repeated motifs, thereby contributing to regulate H3K27me3 homeostasis over the genome.
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Project description:Chromatin architecture relies on histone H1 whose central globular domain (GH1) sits on the nucleosome dyad and carboxy-terminal domain associates with linker DNA. We report that Arabidopsis H1 positively influences H3K27me3 chromatin enrichment over protein-coding genes but oppositely prevents its accumulation on telomeres and heterochromatic Interstitial Telomeric Repeats (ITRs). Contrasting with their neighboring heterochromatic environment, pericentromeric ITR regions remain highly compacted and are more prone to long-distance interactions with telomeres in H1 mutant plants. The switch from H1-rich to H3K27me3-rich ITR chromatin is further accompanied by an invasion of GH1-Myb Telomeric Repeat Binding protein 1 (TRB1), a structural component of telomeres capable to trigger H3K27me3 deposition over protein-coding genes displaying short telomeric motifs. This dual effect led us to propose a competition mechanism between H1 and TRB that prevents massive H3K27me3 deposition over large blocks of repeated motifs, thereby contributing to regulate H3K27me3 homeostasis over the genome.
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