A composite DNA element that functions as a maintainer required for epigenetic inheritance of heterochromatin
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA716976 | ENA |
REPOSITORIES: ENA
Similar Datasets
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
Project description:Epigenetic inheritance of heterochromatin requires sequence - independent propagation mechanisms and input from DNA sequence, but how DNA contributes to inheritance is not understood. Here, we identify a DNA element ( term ed the “maintainer” ) that is necessary and sufficient for epigenetic inheritance of preexisting histone H3 lysine 9 methylation (H3K9me) and heterochromatin i n the fission yeast Schizosaccharomyces pombe . In wild - type cells, d espite its requirement for maintenance of H3K9me, the maintainer cannot establish de novo gene silencing. The maintainer is a composite 1307 - base pair DNA element with binding sites for the Atf1/Pcr1 and Deb1 transcription factors and the O rigin R ecognition C omplex (ORC) and can be converted to a silencer in cells with lower rates of H3K9me turnover , suggesting that it participate s in recruiting the H3K9 methyltransferase Clr4 / Suv39h . T hese results suggest tha t 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 .
2021-08-09 | GSE169537 | GEO
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
Project description: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.
2020-11-18 | GSE150542 | GEO
Project description:RNAi mediates allele-specific epigenetic inheritance of heterochromatin
| PRJNA438361 | ENA
Project description:The INO80 complex regulates epigenetic inheritance of heterochromatin
| PRJNA632735 | ENA
Project description:Heterochromatin domains defined by distinct histone methylation patterns are a major feature of mammalian genomes. Epigenetic pathways ensure stable heterochromatin inheritance through cell division to prevent the expression of lineage-inappropriate genes and defects in this process can lead to many diseases including cancer. Previous studies have shown that heterochromatin maintenance requires a critical threshold of methylated histones, but how modified parental histones are transferred to daughter strands during DNA replication is unclear. We find that heterochromatin domains are specialized replication zones enriched in replisome components, which load factors that help retain parental histones. This mechanism is further supported by the boundary elements surrounding the heterochromatin domains. DNA replication is thus coordinated with histone preservation to facilitate epigenetic inheritance of heterochromatin.
2024-02-02 | GSE242353 | GEO
Project description:The highly conserved multienzyme Rix1-containing complex (hereafter referred to as the rixosome), is required for ribosomal RNA (rRNA) processing and also localizes to heterochromatin in fission yeast, but its role in heterochromatin formation is unknown. Here we report the isolation of separation of function mutations in subunits of the rixosome that abolish its physical association with Swi6/HP1 and localization to heterochromatin, but do not affect growth or rRNA processing. These mutations abolish the epigenetic inheritance of silencing and histone H3 lysine 9 methylation (H3K9me), accumulate heterochromatic RNAs, and cannot spread H3K9me and silencing away from nucleation sites into an inserted transgene. We further show that the rixosome acts upstream of the conserved 5’-3’ exoribonuclease Dhp1/XRN2 to promote heterochromatic RNA degradation. These findings reveal a new RNA degradation pathway that specifically localizes to heterochromatin to degrade nascent transcripts and enable heterochromatin spreading and inheritance.
2020-06-08 | GSE140920 | GEO
Project description:Heterochromatin is essential in all eukaryotic systems to maintain genome integrity, long-term gene repression and to help chromosome segregation during mitosis. However, heterochromatin regions must be restricted by boundary elements to avoid its spreading over actively transcribed loci. In Plasmodium falciparum, facultative heterochromatin is important to regulate parasite virulence, antigenic variation and transmission, but the underlying molecular mechanisms that regulate repressive regions remain unknown. To investigate this topic, we chose the ap2-g gene, that forms a strictly delimited heterochromatin island of 10 kb with no adjacent repressive chromatin. Using electrophoretic motility shift assay (EMSA) we identified an ap2-g exon element at the 3? end that shifts in the presence of nuclear extracts. Upon replacement of this region by a gfp gene, we observed a shift in the heterochromatin boundary, resulting in HP1 to spread over ~2 additional kb downstream. We used this DNA element to affinity purify candidate proteins followed by liquid-chromatography tandem mass-spectrometry (LC-MS/MS). The identified complexes are enriched in RNA-binding proteins, pointing to a potential role of RNA in the regulation of the ap2-g heterochromatin 3? boundary. Our results provide insight into the unexplored topic of heterochromatin boundary biology in P. falciparum and identifies a DNA element in the master regulator of sexual commitment that modulates heterochromatin spreading.
2020-02-18 | GSE145378 | GEO
Project description:The INO80 complex regulates epigenetic inheritance of heterochromatin (RNA-seq)
| PRJNA632746 | ENA