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Repression of germline genes in C. elegans somatic tissues by H3K9 dimethylation of their promoters [ChIP-seq]

ABSTRACT: Repression of germline genes in C. elegans somatic tissues by H3K9 dimethylation of their promoters [ChIP-seq]

PROVIDER: PRJNA523581 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8602940.fastq.gz	Fastqsanger.gz
	SRR8602950.fastq.gz	Fastqsanger.gz
	SRR8602960.fastq.gz	Fastqsanger.gz
	SRR8602970.fastq.gz	Fastqsanger.gz
	SRR8602980.fastq.gz	Fastqsanger.gz

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Repression of germline genes in C. elegans somatic tissues by H3K9 dimethylation of their promoters

Project description:Repression of germline genes in C. elegans somatic tissues by H3K9 dimethylation of their promoters

| PRJNA523597 | ENA

Repression of Germline Genes in <i>Caenorhabditis elegans</i> Somatic Tissues by H3K9 Dimethylation of Their Promoters.

Project description:Repression of germline-promoting genes in somatic cells is critical for somatic development and function. To study how germline genes are repressed in somatic tissues, we analyzed key histone modifications in three Caenorhabditis elegans synMuv B mutants, lin-15B, lin-35, and lin-37-all of which display ectopic expression of germline genes in the soma. LIN-35 and LIN-37 are members of the conserved DREAM complex. LIN-15B has been proposed to work with the DREAM complex but has not been shown biochemically to be a member of the complex. We found that, in wild-type worms, synMuv B target genes and germline genes are enriched for the repressive histone modification dimethylation of histone H3 on lysine 9 (H3K9me2) at their promoters. Genes with H3K9me2 promoter localization are evenly distributed across the autosomes, not biased toward autosomal arms, as are the broad H3K9me2 domains. Both synMuv B targets and germline genes display a dramatic reduction of H3K9me2 promoter localization in lin-15B mutants, but much weaker reduction in lin-35 and lin-37 mutants. This difference between lin-15B and DREAM complex mutants likely represents a difference in molecular function for these synMuv B proteins. In support of the pivotal role of H3K9me2 in regulation of germline genes by LIN-15B, global loss of H3K9me2 but not H3K9me3 results in phenotypes similar to synMuv B mutants, high-temperature larval arrest, and ectopic expression of germline genes in the soma. We propose that LIN-15B-driven enrichment of H3K9me2 at promoters of germline genes contributes to repression of those genes in somatic tissues.

| S-EPMC6499516 | biostudies-literature

Repression of germline genes in C. elegans somatic tissues by H3K9 dimethylation of their promoters [ChIP-seq]

Project description:synMuv B proteins, including LIN-15B, are necessary to repress the expression of germline-promoting genes in the soma during embryonic and early larval development in C. elegans. The goal of this research was to determine if changes to histone modifications could underlie the misexpression of germline genes in these mutants. We performed ChIP-seq on four histone modifications in wild type and three synMuv B mutants at two temperatures to assess these changes.

2019-02-21 | GSE126871 | GEO

Repression of germline genes in C. elegans somatic tissues by H3K9 dimethylation of their promoters

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-02-22 | GSE126884 | GEO

Regulation of mammalian 3D genome organization and histone H3K9 dimethylation by H3K9 methyltransferases

Project description:Histone H3 lysine 9 dimethylation (H3K9me2) is a highly conserved silencing epigenetic mark. Chromatin marked with H3K9me2 forms large domains in mammalian cells and overlaps well with lamina-associated domains and the B compartment defined by Hi-C. However, the role of H3K9me2 in 3-dimensional (3D) genome organization remains unclear. We investigated genome-wide H3K9me2 distribution, transcriptome, and 3D genome organization in mouse embryonic stem cells following the inhibition or depletion of five H3K9 methyltransferases (MTases): G9a, GLP, SETDB1, SUV39H1, and SUV39H2. H3K9me2 was regulated by all five MTases; however, H3K9me2 and transcription in the A and B compartments were regulated by different MTases. H3K9me2 in A compartments was primarily regulated by G9a/GLP and SETDB1, while H3K9me2 in the B compartments was regulated by all five MTases. Furthermore, decreased H3K9me2 correlated with changes to the more active compartmental state that accompanied transcriptional activation.

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Effects of RNAi protein overexpression in mutant cells on H3K9 dimethylation in fission yeast cells

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Stochastic genome - nuclear lamina contacts are linked to histone H3K9 dimethylation (methylation data)

Project description:The nuclear lamina (NL) interacts with hundreds of large genomic regions termed lamina-associated domains (LADs). The dynamics of these interactions and the relation to epigenetic modifications are poorly understood. We visualized the fate of LADs in single cells using a novel 'molecular contact memory' approach. In each interphase nucleus, only ~30% of LADs are positioned at the periphery; these LADs are in intermittent molecular contact with the NL but remain constrained to the periphery. Upon mitosis, LAD positioning is not detectably inherited but instead is stochastically reshuffled. Contact of individual LADs with the NL correlates with their degree of H3K9 dimethylation in single cells, and inactivation of the H3K9 methyltransferase G9a reduces the NL contact frequencies. These results indicate that nuclear positioning and histone modification of LADs are both stochastic yet linked in single cells. Collectively, these results highlight principles of the dynamic spatial architecture of chromosomes. LaminB1-chromatin interactions were assayed in human HT1080 cells by induction of Dam_LMNB1 expression in a stable cell line with shield1.

2013-01-31 | E-GEOD-40094 | biostudies-arrayexpress

Stochastic genome - nuclear lamina contacts are linked to histone H3K9 dimethylation (methylation data)

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Project description:H3K9 dimethylation safeguards cancer cells against activation of the Interferon pathway [WGBS]

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