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Nuclear peripheral positioning of heterochromatin by Amo1NUPL2 suppresses nucleosome turnover to promote epigenetic inheritance [ChIP-seq]

ABSTRACT: Nuclear peripheral positioning of heterochromatin by Amo1NUPL2 suppresses nucleosome turnover to promote epigenetic inheritance [ChIP-seq]

PROVIDER: PRJNA591922 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10539869.fastq.gz	Fastqsanger.gz
	SRR10539870.fastq.gz	Fastqsanger.gz
	SRR10539871.fastq.gz	Fastqsanger.gz
	SRR10539872.fastq.gz	Fastqsanger.gz
	SRR10539873.fastq.gz	Fastqsanger.gz

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Nuclear peripheral positioning of heterochromatin by Amo1NUPL2 suppresses nucleosome turnover to promote epigenetic inheritance

Project description:Nuclear peripheral positioning of heterochromatin by Amo1NUPL2 suppresses nucleosome turnover to promote epigenetic inheritance

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Snf2 Family Protein Fft3 Suppresses Nucleosome Turnover to Promote Epigenetic Inheritance of Heterochromatin and Proper Replication of the Genome [H3K9me2 ChIP]

Project description:H3K9me2 profiles and Fft3 occupancy in 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.

2017-03-21 | GSE88902 | GEO

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

Project description:H3-FLAG incorporation in Schizosaccharomyces pombe 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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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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The INO80 complex regulates epigenetic inheritance of heterochromatin (RNA-seq)

Project description:One key aspect of epigenetic inheritance is that chromatin structure can be stably inherited through generations even after removal of the initial signal that establishes such structure. In fission yeast, the RNA interference (RNAi) machinery is critical for the targeting of histone methyltransferase Clr4 to repetitive DNA elements to establish a large domain of heterochromatin marked with histone H3 lysine 9 methylation (H3K9me). Subsequently during DNA replication, the deposition of parental histones containing H3K9me into daughter DNA strands is expected to recruit Clr4 to modify neighboring new histones, resulting in the inheritance of heterochromatin in both daughter cells. However, pericentric heterochromatin cannot be properly inherited in the absence of RNAi, suggesting the existence of mechanisms that counteract chromatin-based inheritance. Here we show that in the absence of certain components of the INO80 chromatin remodeling complex, pericentric heterochromatin can be properly inherited in RNAi mutants. The ability of INO80 to counter heterochromatin inheritance is attributed to one accessory subunit Iec5, which promotes histone turn over at heterochromatin regions, but has little effects on the ability of INO80 in regulating nucleosome positioning at heterochromatin, gene expression, or the DNA damage response. Slow histone turnover preserves parental histones at repeat regions to enhance epigenetic inheritance of heterochromatin not only in RNAi mutants but also in wild type cells. Our analyses identified a separation-of-function mutation of INO80 in regulating histone turnover at heterochromatin and demonstrate the important role of histone turnover in controlling heterochromatin inheritance and maintaining the proper heterochromatin landscape of the genome.

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Hrp3 controls nucleosome positioning to suppress non-coding transcription in eu- and heterochromatin

Project description:This SuperSeries is composed of the following subset Series: GSE37697: Antisense Transcripts in Mutant Strains GSE40451: Hrp3 controls nucleosome positioning to suppress non-coding transcription in eu- and heterochromatin [MNase-Seq] Refer to individual Series

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