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Caenorhabditis elegans

ABSTRACT: H3K9me2 and BRCA1 cooperate to prevent satellite repeat transcription, R-loop formation and germline sterility [ChIP-seq]

PROVIDER: PRJNA392973 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5799210_1.fastq.gz	Fastqsanger.gz
	SRR5799210_2.fastq.gz	Fastqsanger.gz
	SRR5799211_1.fastq.gz	Fastqsanger.gz
	SRR5799211_2.fastq.gz	Fastqsanger.gz
	SRR5799202_1.fastq.gz	Fastqsanger.gz

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Caenorhabditis elegans

Project description:H3K9me2 and BRCA1 cooperate to prevent satellite repeat transcription, R-loop formation and germline sterility [RNA-seq]

| PRJNA392972 | ENA

H3K9me2 and BRCA1 cooperate to prevent satellite repeat transcription, R-loop formation and germline sterility

Project description:H3K9me2 and BRCA1 cooperate to prevent satellite repeat transcription, R-loop formation and germline sterility

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H3K9me2 and BRCA1 cooperate to prevent satellite repeat transcription, R-loop formation and germline sterility [ChIP-seq]

Project description:Repetitive sequences, transposable elements and silent tissue-specific genes in C. elegans are differentially enriched for di- and tri-methyl H3 lysine 9 (H3K9). SET-25 (SUV39h1/h2) catalyzes H3K9me3, while MET-2 (SetDB1) deposits only H3K9me1/me2. RNA-seq and genome-wide H3K9 methylation mapping in met-2 and set-25 single mutants showed that H3K9me2-mediated repression of satellite repeats by MET-2 correlates with germline integrity. Aberrant transcription of repeats and DNA transposons generates R-loops, loss of fertility and hydroxyurea hypersensitivity. In a genome-wide synthetic lethal screen, we identified the BRCA1 complex and factors implicated in the degradation of nuclear RNA as essential for germline integrity in met-2 mutants. Highly additive with met-2, the loss of the BRCA1 complex triggers satellite repeat transcription, generating R-loops on transcribed repeats. Supporting direct causality between satellite repeat transcription and BRCA1-mediated genome integrity, the targeted induction of MSAT1 transcripts at endogenous sites leads to damage-induced loss of fertility in wild-type C. elegans.

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H3K9me2 and BRCA1 cooperate to prevent satellite repeat transcription, R-loop formation and germline sterility [RNA-seq]

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Vitamin C Induces Specific Demethylation of H3K9me2 in Mouse Embryonic Stem Cells via Kdm3a/b

Project description:Histone methylation patterns regulate gene expression and are highly dynamic during development. The erasure of histone methylation is carried out by histone demethylase enzymes. We had previously shown that vitamin C enhances the activity of Tet enzymes in embryonic stem (ES) cells, leading to DNA demethylation and activation of germline genes. We report here that vitamin C induces a remarkably specific demethylation of histone H3 lysine 9 dimethylation (H3K9me2) in ES cells. Vitamin C treatment reduces global levels of H3K9me2, but not other histone methylation marks analyzed, as measured by Western blot, immunofluorescence and mass spectrometry. Vitamin C leads to widespread loss of H3K9me2 at large chromosomal domains as well as gene promoters and repeat elements. Vitamin C-induced loss of H3K9me2 occurs rapidly within 24 hours and is reversible. Importantly, we found that the histone demethylases Kdm3a and Kdm3b are required for vitamin C-induced demethylation of H3K9me2. Moreover, we show that vitamin C-induced Kdm3a/b-mediated H3K9me2 demethylation and Tet-mediated DNA demethylation are independent processes. Lastly, we document Kdm3a/b are partially required for the up-regulation of germline genes by vitamin C. These results reveal a specific role for vitamin C in histone demethylation in ES cells, and document that DNA methylation and H3K9me2 cooperate to silence germline genes in pluripotent cells.

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A team of heterochromatin factors collaborates with small RNA pathways to combat repetitive elements and germline stress [RNA-seq]

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A team of heterochromatin factors collaborates with small RNA pathways to combat repetitive elements and germline stress [ChIP-seq]

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Protease-mediated processing of Argonaute proteins controls small RNA association [small RNA RIP-seq]

Project description:Small RNA pathways defend the germlines of animals against selfish genetic elements and help to maintain genomic integrity. At the same time, their activity needs to be well-controlled to prevent silencing of ‘self’ genes. Here, we reveal a proteolytic mechanism that controls endogenous small interfering (22G) RNA activity in the Caenorhabditis elegans germline to protect genome integrity and maintain fertility. We find that WAGO-1 and WAGO-3 Argonaute proteins are produced as pro-proteins that are matured through proteolytic processing of their unusually proline-rich N-termini. In the absence of DPF-3, a P-granule-localized N-terminal dipeptidase orthologous to mammalian DPP8/9, processing fails, causing a change of identity of 22G RNAs bound to these WAGO proteins. Accumulation of repeat- and transposon-derived transcripts, DNA damage and sterility ensue. We propose that DPF-3 acts as a licensing factor for 22G RNA activity.

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Protease-mediated processing of Argonaute proteins controls small RNA association [RIP-Seq]

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