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

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

PROVIDER: PRJNA754386 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15443101_1.fastq.gz	Fastqsanger.gz
	SRR15443101_2.fastq.gz	Fastqsanger.gz
	SRR15443102_1.fastq.gz	Fastqsanger.gz
	SRR15443102_2.fastq.gz	Fastqsanger.gz
	SRR15443103_1.fastq.gz	Fastqsanger.gz

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H3K9 dimethylation safeguards cancer cells against activation of the Interferon pathway

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

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H3K9 dimethylation safeguards cancer cells against activation of the Interferon pathway [RNA-seq]

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

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H3K9 dimethylation safeguards cancer cells against activation of the Interferon pathway [SUV39H1_ChIP-seq]

Project description:H3K9 dimethylation safeguards cancer cells against activation of the Interferon pathway [SUV39H1_ChIP-seq]

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H3K9 dimethylation safeguards cancer cells against activation of the Interferon pathway [ChIP-seq]

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

| PRJNA673461 | ENA

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

Project description:Activation of interferon genes constitutes an important anticancer pathway able to restrict proliferation of cancer cells. Here we demonstrate that the H3K9me3 histone methyl transferase (HMT) Suppressor of Variegation 3-9 Homolog 1 (SUV39H1) is required for the proliferation of Acute Myeloid Leukemia (AML) and find that its loss leads to activation of the interferon pathway. Mechanistically, we show that this occurs via destabilization of a complex composed of SUV39H1 and the two H3K9me2 HMTs, G9A and GLP. Indeed, loss of H3K9me2 correlated with the activation of key interferon pathway genes, and interference with the activities of G9A/GLP largely phenocopied loss of SUV39H1. Finally, we demonstrate that inhibition of G9A/GLP synergized with DNA demethylating agents and that SUV39H1 constitutes a potential biomarker for the response to hypomethylation treatment. Collectively, we uncovered a clinically relevant role for H3K9me2 in safeguarding cancer cells against activation of the interferon pathway.

2022-03-18 | GSE182056 | GEO

H3K9 dimethylation safeguards cancer cells against activation of the Interferon pathway [SUV39H1_ChIP-seq]

Project description:Activation of the interferon genes constitutes an important anticancer pathway, able to restrict proliferation of cancer cells. Here we demonstrate that the H3K9me3 histone methyl transferase (HMT) Suppressor Of Variegation 3-9 Homolog 1 (SUV39H1) is required for the proliferation of Acute Myeloid Leukemia (AML) and find that its loss leads to activation of the interferon pathway. Mechanistically, we show that this occur via destabilization of a complex composed of SUV39H1 and the two H3K9me2 HMTs G9a and GLP. Indeed, loss of H3K9me2 correlated with the activation of key interferon pathway genes and interference with the activities of G9a/GLP largely phenocopied loss of SUV39H1. Finally, we demonstrated that inhibition of G9a/GLP synergized with DNA demethylating agents and that SUV39H1 constitutes a potential biomarker the response to hypomethylation treatment. Collectively, we uncovered a clinical relevant role for H3K9me2 in safeguarding cancer cells against activation of the interferon pathway.

2022-03-18 | GSE190469 | GEO

H3K9 dimethylation safeguards cancer cells against activation of the Interferon pathway [RNA-seq]

2022-03-18 | GSE160531 | GEO

H3K9 dimethylation safeguards cancer cells against activation of the Interferon pathway [ChIP-seq]

2022-03-18 | GSE160530 | 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.

2021-08-05 | PXD024756 | Pride

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

Project description:We test the effects of overexpressing RNAi proteins Dcr1, Rdp1, or Ago1 in wildtype, dcr1M-bM-^HM-^F, ago1M-bM-^HM-^F, or rdp1M-bM-^HM-^F cells. We find that overexpression does not generally affect H3K9me2 at euchromatic loci, but there are varying effects in H3K9me2 on centromeric heterochromatin. Examination of genome-wide enrichment in H3K9 dimethylation in fission yeast haploid cells

2013-12-26 | E-GEOD-52444 | biostudies-arrayexpress

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