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Germline inheritance of H3K9me3 and its function in constitutive heterochromatin establishment.[CUT&Tag]

ABSTRACT: Germline inheritance of H3K9me3 and its function in constitutive heterochromatin establishment.[CUT&Tag]

PROVIDER: PRJNA1003940 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25591607_1.fastq.gz	Fastqsanger.gz
	SRR25591607_2.fastq.gz	Fastqsanger.gz
	SRR25591608_1.fastq.gz	Fastqsanger.gz
	SRR25591608_2.fastq.gz	Fastqsanger.gz
	SRR25591609_1.fastq.gz	Fastqsanger.gz

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Germline inheritance of H3K9me3 and its function in constitutive heterochromatin establishment. [GRO-seq]

Project description:Germline inheritance of H3K9me3 and its function in constitutive heterochromatin establishment. [GRO-seq]

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Germline inheritance of H3K9me3 and its function in constitutive heterochromatin establishment. [GRO-seq]

Project description:To investigate the function of H3K9me3 in constitutive heterochromatin formation in early embryo we have created embryos that are devoid of H3K9me3

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Germline inheritance of H3K9me3 and its function in constitutive heterochromatin establishment.[CUT&Tag]

Project description:To investigate the function of H3K9me3 in constitutive heterochromatin formation in early embryo we have created embryos that are devoid of H3K9me3

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Requirements for Establishment and Epigenetic Inheritance of Mammalian Heterochromatin

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LSD1 Prevents Aberrant Heterochromatin Formation in Neurospora crassa

Project description:Heterochromatin is a specialized form of chromatin that restricts access to DNA and inhibits genetic processes, including transcription and recombination. In Neurospora crassa, constitutive heterochromatin is characterized by trimethylation of lysine 9 on histone H3, hypoacetylation of histones, and DNA methylation. Here we explore whether the conserved histone demethylase, lysine-specific demethylase 1 (LSD1), regulates heterochromatin in Neurospora, and if so, how. Though LSD1 is implicated in heterochromatin regulation, its function is inconsistent across different systems; orthologs of LSD1 have been shown to either promote or antagonize heterochromatin expansion by removing H3K4me or H3K9me respectively. We identify three members of the Neurospora LSD complex (LSDC): LSD1, PHF1, and BDP-1, and strains deficient for any exhibit variable spreading of heterochromatin and establishment of new heterochromatin domains dispersed across the genome. Heterochromatin establishment outside of canonical domains in Neurospora share the unusual characteristic of DNA methylation-dependent H3K9me3; typically, H3K9me3 establishment is independent of DNA methylation. Consistent with this, the hyper-H3K9me3 phenotype of LSD1 knock-out strains is dependent on the presence of DNA methylation, as well as HCHC-mediated histone deacetylation, suggesting spreading is dependent on some feedback mechanism. Altogether, our results suggest LSD1 works in opposition to HCHC to maintain proper heterochromatin boundaries.

2021-07-21 | PXD017300 | Pride

Requirements for Establishment and Epigenetic Inheritance of Mammalian Heterochromatin [CRISPR Screen]

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Requirements for Establishment and Epigenetic Inheritance of Mammalian Heterochromatin [ChIP-Seq]

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Loss of HP1 causes depletion of H3K27me3 from facultative heterochromatin and gain of H3K27me2 at constitutive heterochromatin

Project description:Methylated lysine 27 on histone H3 (H3K27me) marks repressed "facultative heterochromatin", including developmentally regulated genes in plants and animals. The mechanisms responsible for localization of H3K27me are largely unknown, perhaps in part because of the complexity of epigenetic regulatory networks. We used a relatively simple model organism bearing both facultative and constitutive heterochromatin, Neurospora crassa, to explore possible interactions between elements of heterochromatin. In higher eukaryotes, reductions of H3K9me3 and DNA methylation in constitutive heterochromatin have been variously reported to cause redistribution of H3K27me3. In Neurospora, we found that elimination of any member of the DCDC H3K9 methylation complex (DIM-5, DIM-7, CUL4, DDB1/DIM-8 or DIM-9) caused massive changes in the distribution of H3K27me; regions of facultative heterochromatin lost H3K27me3 while regions that are normally marked by H3K9me3 became methylated at H3K27. Elimination of DNA methylation by deletion of the DNA methyltransferase gene, dim-2, had no obvious effect on the distribution of H3K27me. Elimination of HP1, which "reads" H3K9me3, also caused major changes in the distribution of H3K27me, indicating that HP1 is important for normal localization of facultative heterochromatin. Because loss of HP1 caused redistribution of H3K27me2/3 but not H3K9me3, these normally non-overlapping marks became superimposed. Indeed, mass spectrometry revealed substantial cohabitation of H3K9me3 and H3K27me2 on H3 molecules from an hpo strain. Loss of H3K27me machinery (e.g. the methyltransferase SET-7) did not impact constitutive heterochromatin, but partially rescued the slow growth of the DCDC mutants, suggesting that the poor growth of these mutants is partly attributable to ectopic H3K27me. Altogether, our findings with Neurospora clarify interactions of facultative and constitutive heterochromatin in eukaryotes.

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Mkt1 is required for RNAi-mediated silencing and establishment of heterochromatin in fission yeast

Project description:Constitutive domains of repressive heterochromatin are maintained within the fission yeast genome through self-reinforcing mechanisms involving histone methylation and small RNAs. Non-coding RNAs generated from heterochromatic regions are processed into small RNAs by the RNA interference pathway, and are subject to silencing through both transcriptional and post-transcriptional mechanisms. While the pathways involved in maintenance of the repressive heterochromatin state are reasonably well understood, less is known about the requirements for its establishment. Here we describe a novel role for the post-transcriptional regulatory factor Mkt1 in establishment of heterochromatin at pericentromeres in fission yeast. Loss of Mkt1 does not affect maintenance of existing heterochromatin, but does affect its recovery following depletion, as well as de novo establishment of heterochromatin on a mini-chromosome. Pathway dissection revealed that Mkt1 is required for RNAi-mediated post-transcriptional silencing, downstream of small RNA production. Mkt1 physically associates with pericentromeric transcripts, and is additionally required for maintenance of silencing and heterochromatin at centromeres when transcriptional silencing is impaired. Our findings provide new insight into the mechanism of RNAi-mediated post-transcriptional silencing in fission yeast, and unveil an important role for post-transcriptional silencing in establishment of heterochromatin that is dispensable when full transcriptional silencing is imposed.

2019-11-28 | PXD015484 | Pride

Repetitive sequences drive the condensation of H3K9me3 Methyltransferase complex to promote epigenetic inheritance in Caenorhabditis elegans [transgenes]

Project description:Histone H3K9 trimethylation (H3K9me3) plays a pivotal role in the establishment and maintenance of heterochromatin and is essential for facilitating epigenetic inheritance. H3K9me3 is often biasedly deposited and associated with repetitive sequence region, although the underlying mechanism remain poorly understood. In this study, we identify two proteins, SECP-1 and SECP-2, as crucial cofactors for the genome-wide deposition of H3K9me3 in Caenorhabditis elegans. SECP-1 interacts directly with SECP-2 and the primary H3K9me3 methyltransferase, SET-25, forming a protein complex that bridges SECP-2 with SET-25. This complex assembles in the cytoplasm and is transported into the nucleus through SET-25. Once in the nucleus, the complex is recruited to and concentrated at SET-25’s genomic targets in an interdependent manner. The accumulation of this complex correlates with the formation of condensates at repetitive sequences, the perinuclear localization of heterochromatin, and the epigenetic inheritance of small RNA-mediated gene silencing. The introduction of transgenic arrays leads to the redistribution of the SECP-1/SECP-2/SET-25 complex to the transgene locus, a genome-wide decrease in H3K9me3 levels, and an increase in repetitive sequence expression. We propose that repetitive sequences drive the formation of condensates containing H3K9me3 methyltransferase complexes, which in turn causes a biased deposition of H3K9me3 at these genomic regions.

2025-05-28 | GSE297992 | GEO

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