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RNAi promotes heterochromatic silencing through replication-coupled release of RNA pol II (RNA seq)

ABSTRACT: Heterochromatin comprises tightly compacted repetitive regions of eukaryotic chromosomes. The inheritance of heterochromatin through mitosis requires RNA interference (RNAi), which guides histone modification during the DNA replication phase of the cell cycle. Here, we show that the alternating arrangement of origins of replication and non-coding RNA in pericentromeric heterochromatin results in competition between transcription and replication. Co-transcriptional RNAi releases RNA polymerase II (PolII), allowing completion of DNA replication by the leading strand DNA polymerase, and associated histone modifying enzymes which spread heterochromatin with the replication fork. In the absence of RNAi, stalled forks are repaired by homologous recombination without histone modification.

ORGANISM(S): Schizosaccharomyces pombe

PROVIDER: GSE30827 | GEO | 2011/07/21

SECONDARY ACCESSION(S): PRJNA154563

REPOSITORIES: GEO

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RNAi promotes heterochromatic silencing through replication-coupled release of RNA pol II (RNA seq)

Project description:Heterochromatin comprises tightly compacted repetitive regions of eukaryotic chromosomes. The inheritance of heterochromatin through mitosis requires RNA interference (RNAi), which guides histone modification during the DNA replication phase of the cell cycle. Here, we show that the alternating arrangement of origins of replication and non-coding RNA in pericentromeric heterochromatin results in competition between transcription and replication. Co-transcriptional RNAi releases RNA polymerase II (PolII), allowing completion of DNA replication by the leading strand DNA polymerase, and associated histone modifying enzymes which spread heterochromatin with the replication fork. In the absence of RNAi, stalled forks are repaired by homologous recombination without histone modification. small RNA cloning from wild type and dcr1-deleted strains

2011-07-21 | E-GEOD-30827 | biostudies-arrayexpress

RNAi promotes heterochromatic silencing through replication-coupled release of RNA pol II (ChIP-seq)

Project description:Heterochromatin comprises tightly compacted repetitive regions of eukaryotic chromosomes. The inheritance of heterochromatin through mitosis requires RNA interference (RNAi), which guides histone modification 1 during the DNA replication phase of the cell cycle2. Here, we show that the alternating arrangement of origins of replication and non-coding RNA in pericentromeric heterochromatin results in competition between transcription and replication. Co-transcriptional RNAi releases RNA polymerase II (PolII), allowing completion of DNA replication by the leading strand DNA polymerase, and associated histone modifying enzymes3 which spread heterochromatin with the replication fork. In the absence of RNAi, stalled forks are repaired by homologous recombination without histone modification. RNA PolII ChIP from wild type and dcr1-deleted samples in exponentially growing and HU-arrested cultures.

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RNAi promotes heterochromatic silencing through replication-coupled release of RNA pol II (ChIP-seq)

Project description:Heterochromatin comprises tightly compacted repetitive regions of eukaryotic chromosomes. The inheritance of heterochromatin through mitosis requires RNA interference (RNAi), which guides histone modification 1 during the DNA replication phase of the cell cycle2. Here, we show that the alternating arrangement of origins of replication and non-coding RNA in pericentromeric heterochromatin results in competition between transcription and replication. Co-transcriptional RNAi releases RNA polymerase II (PolII), allowing completion of DNA replication by the leading strand DNA polymerase, and associated histone modifying enzymes3 which spread heterochromatin with the replication fork. In the absence of RNAi, stalled forks are repaired by homologous recombination without histone modification.

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The Mi-2 homolog, Mit1, actively positions nucleosomes within heterochromatic domains to suppress transcription

Project description:Nucleosome positioning is both active and passive and regulates access to the genome for replication, transcription and repair. Here we report that Mit1, a subunit of the fission yeast SHREC complex similar to Mi-2/NuRD, regulates transcription at regions of heterochromatin by positioning nucleosomes to preclude access to RNA Polymerase II. Purified Mit1 is a nucleosome remodeling factor capable of mobilizing histone octamers on short DNA fragments and requires ATP hydrolysis and chromatin tethering domains to remodel nucleosomes and silence transcription. We propose that SHREC is recruited to heterochromatin to mobilize nucleosomes onto unfavorable positions to prevent spurious transcription within heterochromatin.

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The Mi-2 homolog, Mit1, actively positions nucleosomes within heterochromatic domains to suppress transcription

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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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Examination of H3K27me3 histone modification in 3 cell types in presence or absence of SuUR mutation

Project description:Heterochromatin contains repressively modified histones and replicates late in S phase of the cell cycle. Besides the shortage in replication origins, little is known about replication timing regulation in silenced regions. In Drosophila polytene cells, late replication results in under-replication and decreased DNA copy number in heterochromatic regions of the genome. The Suppressor of Under-replication (SUUR) protein controls this feature â in its absence the DNA polytenization level in most silenced regions is restored, however the repressive histone marks are lost. We hypothesized that SUUR regulates the re-establishment of repressive histone pattern during replication which results in delayed replication completion of heterochromatin. Measuring DNA copy number in mutants with disrupted repressive pathways, we found that under-replication is directly linked to repressive histone marks supply. DamID-seq and ChIP-seq experiments revealed that SuUR mutation does not affect the establishment of heterochromatin domains. Here, we identified a novel SUUR protein interaction (CG12018) that supports SUUR association with replication complex. SUUR loads onto replication forks shortly after the origin firing and participates in chromatin maintenance rather than its establishment. Thus, our findings provide comprehensive evidence that late replication in Drosophila is caused by the time-consuming process of replication-coupled repressive chromatin renewal. Examination of H3K27me3 histone modification in 3 cell types in presence or absence of SuUR mutation.

2016-01-10 | E-GEOD-74908 | biostudies-arrayexpress

ChIP-seq of histone marks (H3K27me1, H3K27me3, H3K9me2) and of the H2A.W histone variant in Arabidopsis pol2a mutants.

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2020-10-18 | E-MTAB-9046 | biostudies-arrayexpress

A Composite DNA Element that Functions as a Maintainer Required for Epigenetic Inheritance of Heterochromatin

Project description:Epigenetic inheritance of heterochromatin requires DNA sequence-independent propagation mechanisms, coupling to RNAi, or input from DNA sequence, but how DNA contributes to inheritance is not understood. Here, we identify a DNA element (termed “maintainer”) that is sufficient for epigenetic inheritance of preexisting histone H3 lysine 9 methylation (H3K9me) and heterochromatin in Schizosaccharomyces pombe, but cannot establish de novo gene silencing in wild-type cells. This maintainer is a composite DNA element with binding sites for the Atf1/Pcr1 and Deb1 transcription factors and the Origin Recognition Complex (ORC), located within a 130-base pair region, and can be converted to a silencer in cells with lower rates of H3K9me turnover, suggesting that it participates in recruiting the H3K9 methyltransferase Clr4/Suv39h. These results suggest that, in the absence of RNAi, histone H3K9me is only heritable when it can collaborate with maintainer-associated DNA-binding proteins that help recruit the enzyme responsible for its epigenetic deposition.

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