RNAi mediates allele-specific epigenetic inheritance of heterochromatin
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA438361 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6837050.fastq.gz | Fastqsanger.gz | |||
| SRR6837060.fastq.gz | Fastqsanger.gz | |||
| SRR6837070.fastq.gz | Fastqsanger.gz | |||
| SRR6837080.fastq.gz | Fastqsanger.gz | |||
| SRR6837120.fastq.gz | Fastqsanger.gz |
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Project description:RNAi mediates allele-specific epigenetic inheritance of heterochromatin [ChIP-seq]
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Project description:RNAi mediates allele-specific epigenetic inheritance of heterochromatin [ncRNA-seq]
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Project description:We tested the ability of trans siRNAs to establish a silent allele of endogenous ade6+ or an ade6+ transgene inserted within euchromatic loci. We found that a silent ade6-OFF epi-allele that grows red on low adenine medium could be established in several mutant backgrounds (mlo3∆, leo1∆) in the presence of ectopic siRNAs. Furthermore, we found that the silent ade6-OFF epi-allele could be meiotically inherited to wildtype progeny lacking the establishing mutation or ectopic siRNAs. Here, we sequenced genome-wide DNA associated with conserved heterochromatin markers and found that silencing of the endogenous ade6 locus correlates with increased spreading of H3K9me2 and H3K9me3. Additionally, heterochromatin domains established with cen::ade6 as the ectopic siRNA-producing locus were associated with significantly more spreading of H3K9me2 and H3K9me3 than those established using an ade6 hairpin as the driver siRNA-producing locus.
2018-04-26 | GSE111851 | GEO
Project description:We tested the ability of trans siRNAs to establish a silent allele of endogenous ade6+ or an ade6+ transgene inserted within euchromatic loci. We found that a silent ade6-OFF epi-allele that grows red on low adenine medium could be established in several mutant backgrounds (mlo3∆, leo1∆) in the presence of ectopic siRNAs. Furthermore, we found that the silent ade6-OFF epi-allele could be meiotically inherited to wildtype progeny lacking the establishing mutation or ectopic siRNAs. Here, we sequenced genome-wide small RNAs and found widespread generation of secondary siRNAs at genes surrounding the ade6-OFF locus in cells expressing the ectopic siRNAs source cen::ade6. In wildtype meiotic progeny lacking the driver cen::ade6 siRNAs, we observed establishment of a local siRNA producing locus at genes adjacent to the endogenous ade6-OFF or at a kanMX-ade6-OFF transgene inserted within euchromatic loci. In contrast, spreading of secondary siRNAs was limited or nonexistent in ade6-ON cells. Finally, we found that spreading of secondary siRNAs at the endogenous ade6 locus was limited when an ade6 hairpin construct served as the ectopic siRNA driver locus instead of cen::ade6.
2018-04-26 | GSE111858 | GEO
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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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: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:This SuperSeries is composed of the SubSeries listed below.
2018-04-26 | GSE111859 | GEO
Project description:Gene silencing mediated by dsRNA (RNAi) can persist for multiple generations in C. elegans (termed RNAi inheritance). Here we describe the results of a forward genetic screen in C. elegans that has identified six factors required for RNAi inheritance: GLH-1/VASA, PUP-1/CDE-1, MORC-1, SET-32, and two novel nematode-specific factors that we term here (heritable RNAi defective) HRDE-2 and HRDE-4. The new RNAi inheritance factors exhibit mortal germline (Mrt) phenotypes, which we show is likely caused by epigenetic deregulation in germ cells. We also show that HRDE-2 contributes to RNAi inheritance by facilitating the binding of small RNAs to the inheritance Argonaute (Ago) HRDE-1. Together, our results identify additional components of the RNAi inheritance machinery whose sequence conservation provides insights into the molecular mechanism of RNAi inheritance, further our understanding of how the RNAi inheritance machinery promotes germline immortality, and show that HRDE-2 couples the inheritance Ago HRDE-1 with the small RNAs it needs to direct RNAi inheritance and germline immortality.
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Project description:PRC2 mediates paternal epigenetic inheritance
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