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The INO80 complex regulates epigenetic inheritance of heterochromatin (ChIP-seq, Mnase-seq)

ABSTRACT: One key aspect of epigenetic inheritance is that chromatin structure can be stably inherited through generations even after removal of the signal that establishes such structure. In fission yeast, the RNA interference (RNAi) machinery is critical for initial targeting of histone methyltransferase Clr4 to pericentric repeats to establish heterochromatin. However, pericentric heterochromatin cannot be properly inherited in the absence of RNAi, suggesting the existence of mechanisms that counteract chromatin structure 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 turnover at heterochromatin regions, but has little effects on 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 demonstrate the importance of INO80 in controlling heterochromatin inheritance and maintaining the proper heterochromatin landscape of the genome.

ORGANISM(S): Schizosaccharomyces pombe

PROVIDER: GSE150542 | GEO | 2020/11/18

REPOSITORIES: GEO

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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.

2020-11-18 | GSE150544 | GEO

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.

2022-10-14 | PXD027214 | Pride

Silencing of pericentric heterochromatin associated with SIRT6-dependent H3K18 deacetylation protects against mitotic errors and cellular senescence

Project description:Pericentric heterochromatin silencing at mammalian centromeres is essential for mitotic fidelity and genomic stability. Defective pericentric silencing is observed in senescent cells, aging tissues, and mammalian tumors, but the underlying mechanisms and functional consequences of these defects are unclear. Here, we uncover a pivotal role of the human SIRT6 enzyme in pericentric transcriptional silencing, and this function protects against mitotic defects, genomic instability, and cellular senescence. At pericentric heterochromatin, SIRT6 promotes deacetylation of a new substrate, histone H3 lysine K18 (H3K18), and inactivation of SIRT6 in cells leads to H3K18 hyperacetylation and aberrant accumulation of pericentric transcripts. Strikingly, RNAi-depletion of these transcripts rescues the mitotic and senescence phenotypes of SIRT6-deficient cells. Together, our findings reveal a new function for SIRT6 and H3K18Ac regulation at heterochromatin, and demonstrate the pathogenic role of de-regulated pericentric transcription in aging- and cancer- related cellular dysfunction. H3K18ac, H3K9ac, H3K9me3, H3K56ac and Input ChIP-seq for U2OS cell

2016-04-04 | E-GEOD-69809 | biostudies-arrayexpress

H3K64me3 and H3K9me3 profiling at promoters in mouse embryonic stem cells

Project description:Histone modifications are central to the regulation of all DNA-dependent processes but the repertoire of known modifications is far from complete. Lysine 64 of Histone H3 (H3K64) lies within the globular domain of H3 at a structurally important position within the nucleosome. We identify tri-methylation of H3K64 (H3K64me3) as a modification enriched in pericentric heterochromatin and associated with repeated sequences and transcriptionally inactive genomic regions. Interestingly, the pericentric enrichment of H3K64me3 depends on the Suv39h methyltransferases. Further, we show that this newly identified mark is dynamically regulated during the two major epigenetic reprogramming events in mammals. In primordial germ cells (PGCs) H3K64me3 is present at the time of specification, but disappears transiently during germline reprogramming. In the early mouse embryo it is inherited exclusively through the maternal germline and specifically enriched in heterochromatic regions of the maternal pronucleus. Subsequently the modification is rapidly removed from the maternal chromatin suggesting an important role for H3K64me3 turnover in development. Taken together, our findings firmly establish H3K64me3 as a novel histone modification mark of repressive chromatin, which displays crosstalk to the Suv39 pathway and is dynamically reprogrammed during development. We hypothesize that methylation of this lysine helps to 'secure' the nucleosome and perhaps the surrounding heterochromatin, in an appropriately repressed state during development. Keywords: ChIP-chip, embryonic stem cells, H3K64me3, H3K9me3, heterochromatin ChIP-chip experiments were performed with four independent biological replicates for H3K64me3 and two independent replicates for H3K9me3. For each condition hybridizations include a dye-swap experiment.

2010-05-16 | E-GEOD-16185 | biostudies-arrayexpress

C. elegans nuclear RNAi factor SET-32 is an H3K23 methyltransferase and deposits the transgenerational heritable modification of H3K23me3

Project description:Nuclear RNAi provides a highly tractable system to study RNA-mediated chromatin changes and epigenetic inheritance. Recent studies indicate that nuclear RNAi-mediated heterochromatin is highly complex in its regulation and function. The knowledge of histone modifications that are involved in nuclear RNAi and the corresponding histone modifying enzymes remains limited. In this study, we show that the heterochromatin mark H3K23me3 is induced by nuclear RNAi at both exogenous and endogenous targets in C. elegans. In addition, RNAi-induced H3K23me3 can be inherited for at least four generations. We also demonstrate that the histone methyltransferase SET-32, methylates H3K23 in vitro. Both set-32 and the germline nuclear RNAi Argonaute, hrde-1, are required for nuclear RNAi-induced H3K23me3 in vivo. Our data poise H3K23me3 as a chromatin modification involved in the nuclear RNAi pathway and provides the field with a new target for uncovering the role of heterochromatin in transgenerational epigenetic silencing.

2020-05-01 | GSE141347 | GEO

Silencing of pericentric heterochromatin associated with SIRT6-dependent H3K18 deacetylation protects against mitotic errors and cellular senescence

2016-04-04 | GSE69809 | GEO

H3K64me3 and H3K9me3 profiling at promoters in mouse embryonic stem cells

2009-06-28 | GSE16185 | GEO

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 (RNA seq)

2011-07-21 | GSE30827 | GEO

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.

2011-07-29 | E-GEOD-31016 | biostudies-arrayexpress

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