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Role of Fft3 in nuclear organization [MNase-seq]

ABSTRACT: In eukaryotic cells, local chromatin structure and chromatin organization in the nucleus both influence transcriptional regulation. At the local level, the Fun30 chromatin remodeler Fft3 is essential for maintaining proper chromatin structure at centromeres and subtelomeres in fission yeast. Using genome-wide mapping and live cell imaging, we show that this role is linked to controlling nuclear organization of its targets. In fft3Δ cells, subtelomeres lose their association with the LEM domain protein Man1 at the nuclear periphery and move to the interior of the nucleus. Furthermore, genes in these domains are upregulated and active chromatin marks increase. Fft3 is also enriched at retrotransposon-derived long terminal repeat (LTR) elements at the borders of subtelomeres and at tRNA genes. In cells lacking Fft3, these sites lose their peripheral positioning and show reduced nucleosome occupancy. We propose that Fft3 has a global role in mediating association between specific chromatin domains and components of the nuclear envelope by maintaining chromatin structure required for anchoring DNA insulators to nuclear pores.

ORGANISM(S): Schizosaccharomyces pombe

PROVIDER: GSE58012 | GEO | 2015/03/02

SECONDARY ACCESSION(S): PRJNA248690

REPOSITORIES: GEO

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Role of Fft3 in nuclear organization [MNase-seq]

Project description:In eukaryotic cells, local chromatin structure and chromatin organization in the nucleus both influence transcriptional regulation. At the local level, the Fun30 chromatin remodeler Fft3 is essential for maintaining proper chromatin structure at centromeres and subtelomeres in fission yeast. Using genome-wide mapping and live cell imaging, we show that this role is linked to controlling nuclear organization of its targets. In fft3M-NM-^T cells, subtelomeres lose their association with the LEM domain protein Man1 at the nuclear periphery and move to the interior of the nucleus. Furthermore, genes in these domains are upregulated and active chromatin marks increase. Fft3 is also enriched at retrotransposon-derived long terminal repeat (LTR) elements at the borders of subtelomeres and at tRNA genes. In cells lacking Fft3, these sites lose their peripheral positioning and show reduced nucleosome occupancy. We propose that Fft3 has a global role in mediating association between specific chromatin domains and components of the nuclear envelope by maintaining chromatin structure required for anchoring DNA insulators to nuclear pores. For MNase samples, duplicate mutant mononucleosome fractions were compared with duplicate WT mononucleosomes.

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Role of Fft3 in nuclear organization [DamID-chip, ChIP-chip]

Project description:In eukaryotic cells, local chromatin structure and chromatin organization in the nucleus both influence transcriptional regulation. At the local level, the Fun30 chromatin remodeler Fft3 is essential for maintaining proper chromatin structure at centromeres and subtelomeres in fission yeast. Using genome-wide mapping and live cell imaging, we show that this role is linked to controlling nuclear organization of its targets. In fft3Δ cells, subtelomeres lose their association with the LEM domain protein Man1 at the nuclear periphery and move to the interior of the nucleus. Furthermore, genes in these domains are upregulated and active chromatin marks increase. Fft3 is also enriched at retrotransposon-derived long terminal repeat (LTR) elements at the borders of subtelomeres and at tRNA genes. In cells lacking Fft3, these sites lose their peripheral positioning and show reduced nucleosome occupancy. We propose that Fft3 has a global role in mediating association between specific chromatin domains and components of the nuclear envelope by maintaining chromatin structure required for anchoring DNA insulators to nuclear pores.

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Role of Fft3 in nuclear organization [DamID-chip, ChIP-chip]

Project description:In eukaryotic cells, local chromatin structure and chromatin organization in the nucleus both influence transcriptional regulation. At the local level, the Fun30 chromatin remodeler Fft3 is essential for maintaining proper chromatin structure at centromeres and subtelomeres in fission yeast. Using genome-wide mapping and live cell imaging, we show that this role is linked to controlling nuclear organization of its targets. In fft3M-NM-^T cells, subtelomeres lose their association with the LEM domain protein Man1 at the nuclear periphery and move to the interior of the nucleus. Furthermore, genes in these domains are upregulated and active chromatin marks increase. Fft3 is also enriched at retrotransposon-derived long terminal repeat (LTR) elements at the borders of subtelomeres and at tRNA genes. In cells lacking Fft3, these sites lose their peripheral positioning and show reduced nucleosome occupancy. We propose that Fft3 has a global role in mediating association between specific chromatin domains and components of the nuclear envelope by maintaining chromatin structure required for anchoring DNA insulators to nuclear pores. For DamID samples, we recorded methylation levels for Dam fusion proteins and compared them to Dam-only control samples. For ChIP samples, we compared immuno-precipitated DNA to mock or input controls.

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The FUN30 Chromatin Remodeler Fft3 Protects Centromeric and Subtelomeric Domains from Euchromatin Formation

Project description:The chromosomes of eukaryotes are organized into structurally and functionally discrete domains. This implies the presence of insulator elements that separate adjacent domains, allowing them to maintain different chromatin structures. We show that the Fun30 chromatin remodeler, Fft3, is essential for maintaining a proper chromatin structure at centromeres and subtelomeres. Fft3 is localized to insulator elements and inhibits euchromatin assembly in silent chromatin domains. In its absence, euchromatic histone modifications and histone variants invade centromeres and subtelomeres, causing a mis-regulation of gene expression and severe chromosome segregation defects. Our data strongly suggest that Fft3 controls the identity of chromatin domains by protecting these regions from euchromatin assembly.

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Role of Fft3 in nuclear organization

Project description:Role of Fft3 in nuclear organization

| PRJNA248689 | ENA

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Snf2 Family Protein Fft3 Suppresses Nucleosome Turnover to Promote Epigenetic Inheritance of Heterochromatin and Proper Replication of the Genome [H3-FLAG ChIP]

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Snf2 Family Protein Fft3 Suppresses Nucleosome Turnover to Promote Epigenetic Inheritance of Heterochromatin and Proper Replication of the Genome [BrdU IP]

Project description:BrdU profiling of replication activity in hydroxyurea treated synchronous culture of fission yeast. Heterochromatin can be epigenetically inherited in cis, leading to stable maintenance of gene expression states. However, the mechanisms underlying heterochromatin inheritance remain unclear. Here we identify Fft3, a homolog of the mammalian SMARCAD1 Snf2 chromatin remodeler, as a factor uniquely required for heterochromatin inheritance, rather than for de novo assembly. Importantly, we find that Fft3 bound to heterochromatic loci suppresses turnover of parental histones and is critical for the epigenetic transmission of heterochromatin in cycling cells. Surprisingly, Fft3 also localizes to several euchromatic loci where it is required for proper replication progression. Fft3 promotes nucleosome stability at these loci to prevent R-loop formation that can impede replication machinery. Strikingly, overexpression of the Clr4/Suv39h methyltransferase, which is also required for efficient replication through these loci, suppresses phenotypes associated with the loss of Fft3. Thus, we find that Fft3 promotes nucleosome stability to facilitate heterochromatin inheritance and also acts in parallel to Clr4 ensure proper replication of euchromatic regions.

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LEM-2 ChIP-seq to study chromatin anchoring

Project description:Chromatin Immunoprecipitation against the nuclear envelope protein LEM-2 to detect association to the nuclear periphery. LEM-2 ChIP was performed on early embryo fixed extracts for wild-type and two mutants that have altered position of a perinuclear chromatin reporter.

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Snf2 Family Protein Fft3 Suppresses Nucleosome Turnover to Promote Epigenetic Inheritance of Heterochromatin and Proper Replication of the Genome [HU + BrdU IP]

Project description:BrdU profiling of replication activity in synchronous culture of fission yeast. Heterochromatin can be epigenetically inherited in cis, leading to stable maintenance of gene expression states. However, the mechanisms underlying heterochromatin inheritance remain unclear. Here we identify Fft3, a homolog of the mammalian SMARCAD1 Snf2 chromatin remodeler, as a factor uniquely required for heterochromatin inheritance, rather than for de novo assembly. Importantly, we find that Fft3 bound to heterochromatic loci suppresses turnover of parental histones and is critical for the epigenetic transmission of heterochromatin in cycling cells. Surprisingly, Fft3 also localizes to several euchromatic loci where it is required for proper replication progression. Fft3 promotes nucleosome stability at these loci to prevent R-loop formation that can impede replication machinery. Strikingly, overexpression of the Clr4/Suv39h methyltransferase, which is also required for efficient replication through these loci, suppresses phenotypes associated with the loss of Fft3. Thus, we find that Fft3 promotes nucleosome stability to facilitate heterochromatin inheritance and also acts in parallel to Clr4 ensure proper replication of euchromatic regions.

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