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.
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.
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.
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.
Project description:Telomere is a highly refined system for maintaining the stability of linear chromosomes. Most telomeres rely on simple repetitive sequences and telomerase enzymes, but in some species or telomerase-defective situations, alternative telomere lengthening (ALT) mechanism is utilized to protect chromosomal ends. Telomere loss can induce telomere recombination by which specific sequences can be recruited into telomeres. However, canonical telomeric repeat-based telomeres have been found in mammals. Here, we show that mammalian telomeres can also be completely reconstituted using a non-telomeric unique sequence. We found that a specific subtelomeric element, named as mouse template for ALT (mTALT), is utilized for repairing telomeric DNA damage and composing new telomeric sequences in mouse embryonic stem cells. We found a high-level of non-coding mTALT transcript despite the heterochromatic nature of mTALT-based telomere. After ALT activation, the increased HMGN1, a non-histone chromosomal protein, contributed to maintaining telomere stability by regulating telomeric transcriptions. Our findings reveal novel molecular features of potential telomeric sequences which can reconstitute telomeres during cancer formation and evolution.
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.
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.
Project description:Centromeric repetitive DNA sequences are highly variable during evolution, which are the hub for genome stability in almost all the eukaryotic organisms. However, how centromeric repeat sequences diverge rapidly among closely related species and populations, and how polyploidy contributed to the diversity of centromere among co-evolved subgenomes are largely unknown. Here, we applied the Brachypodium system to investigate the track of centromere evolution within this taxa, and their adaptation to alloploidization process. Subgenome divergent centromeric satellite repeat were discovered in tetraploid B. hybridum, and this divergent was originated form their two diploid progenitors. Furthermore, differential sequences influence the association sites with CENH3 nucleosomes on the monomer satellite repeats, and positioning of CENH3 nucleosomes on the satellite DNA are stable in each subgenome after alloploidization. Only minor intrasubgenomic variations were observed on these satellite repeats from diploid to tetraploid in B. hybridum, and no evident intersubgenomic transfer of centromeric satellite repeats after alloploidization. Pan-genome analysis reveals that the general principle of centromere dynamic within the populations in Brachypodium genomes with different polyploidy level. Our results provide an unprecedented information regarding the genomic and functional diversity of centromeric repeat DNA during evolution.
Project description:The study of the proteins that bind to telomeric DNA in mammals has provided a deep understanding of the mechanisms of chromosome-end protection. However, very little is known on the binding of these proteins to nontelomeric DNA sequences. The TTAGGG DNA repeat proteins 1 and 2 (TRF1 and TRF2) bind to mammalian telomeres as part of the shelterin complex and are essential for maintaining chromosome end stability. In this study, we combined chromatin immunoprecipitation with high-throughput sequencing to map at high sensitivity and resolution, the human chromosomal sites to which TRF1 and TRF2 bind. While most of the identified sequences correspond to telomeric regions, we showed that these two proteins also bind to extratelomeric sites. The vast majority of these extra-telomeric sites contains interstitial telomeric sequences (or ITSs). However we also identified non-ITS sites, which are also satellite DNA but the ones mainly constitutive of centromeric and pericentromeric regions. Interestingly, the TRF-binding sites are often located in the proximity of genes or within introns. We propose that, by binding to extratelomeric sequences, TRF1 and TRF2 couple the functional state of telomeres to the long-range organization of chromosomes and gene regulation networks. ChIP-SEQ experiment of transformed human fibroblast BJ cells with 3 antibodies (1 monoclonal anti-TRF1, 1 monoclonal anti-TRF2, 1 polyclonal anti-TRF2) and a negative control (proteinG without antibody used as the ChIP background)