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RTEL1 is involved in transcriptional gene silencing and inhibition of heterochromatic DNA methylation

ABSTRACT: RTEL1 is involved in transcriptional gene silencing and inhibition of heterochromatic DNA methylation

PROVIDER: PRJNA811184 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18172047.fastq.gz	Fastqsanger.gz
	SRR18172048.fastq.gz	Fastqsanger.gz
	SRR18172049.fastq.gz	Fastqsanger.gz
	SRR18172050_1.fastq.gz	Fastqsanger.gz
	SRR18172050_2.fastq.gz	Fastqsanger.gz

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Similar Datasets

RTEL1 is involved in transcriptional gene silencing and inhibition of heterochromatic DNA methylation

Project description:Transcriptional gene silencing is an essential mechanism for controlling the expression of genes and transposable elements (TEs) and is commonly associated with high levels of DNA methylation. Thus, release of silencing is frequently observed in mutants for genes involved in DNA methylation maintenance. However, studies in Arabidopsis thaliana have revealed that transcriptional repression of some DNA-methylated genes and TEs also relies on repressors that operate through pathways largely independent of DNA methylation. One such pathway appears linked to DNA replication and DNA repair and mutations in factors involved in these processes such as the polymerases alpha, delta and epsilon destabilize silencing. Here, we isolate a new mutant allele of the helicase REGULATOR OF TELOMERE ELONGATION 1 (RTEL1) gene from a genetic screen for TGS-deficient mutants. RTEL1 is highly conserved among eukaryotes and plays an important role in the resolution of DNA secondary structures during DNA replication. We show that rtel1 causes release of TGS without loss of DNA methylation or global changes in chromatin accessibility. However, many heterochromatic loci show increased levels of DNA methylation and chromatin accessibility in rtel1 mutants. Our findings reveal a function for RTEL1 in maintaining silencing and in preventing DNA hypermethylation of heterochromatin.

2023-07-04 | GSE197614 | GEO

RTEL1 modulates H3 occupancy in heterochromatic regions and acts synergistically with MET1/DDM1 to maintain genome integrity

Project description:RTEL1 mainly mediates histone H3 occupancy in heterochromatic regions and functions in parallel with DDM1 and MET1 to maintain genome integrity.

2019-09-06 | GSE86447 | GEO

Accumulation of RNA on chromatin disrupts heterochromatic silencing

Project description:Long non-coding RNAs (lncRNAs) play a conserved role in regulating gene expression, chromatin dynamics and cell differentiation. They serve as a platform for RNA interference (RNAi)-mediated heterochromatin formation or DNA methylation in many eukaryotic organisms. We found in Schizosaccharomyces pombe, that heterochromatin is lost at transcribed regions in absence of RNA degradation, although establishment is not affected. We show that heterochromatic RNAs accumulate on chromatin, form R-loops and need to be degraded by the Ccr4-Not complex or RNAi to maintain heterochromatic silencing. The Ccr4-Not complex is localized to chromatin independently of H3K9me and degrades chromatin associated transcripts, which is required for transcriptional silencing. Overexpression of heterochromatic lncRNA at a heterochromatic locus abolishes silencing of an ade6 reporter in wild type cells. Furthermore, euchromatic lncRNA accumulate on chromatin and this regulates their transcription. Our results demonstrate that chromatin bound RNA interfere with heterochromatin organization and silencing.

2017-04-12 | GSE94129 | GEO

Spt6 is required for heterochromatic silencing in the fission yeast Schizosaccharomyces pombe

Project description:Spt6 is a conserved factor, critically required for several transcription and chromatin related processes. We now show that Spt6 and its binding partner, Iws1, are required for heterochromatic silencing in Schizosaccharomyces pombe. Our studies demonstrate that Spt6 is required for silencing of all heterochromatic loci and that an spt6 mutant has an unusual combination of heterochromatic phenotypes compared to previously studied silencing mutants. Unexpectedly, we find normal nucleosome positioning over heterochromatin and normal levels of histone H3K9 dimethylation. However, we also find greatly reduced levels of H3K9 trimethylation, elevated levels of H3K14 acetylation, and reduced recruitment of several silencing factors. Our evidence suggests that Spt6 plays a role at both the transcriptional and post-transcriptional levels; in an spt6 mutant, RNA polymerase II (RNAPII) occupancy at the pericentric regions is only modestly increased, while production of small interfering RNAs (siRNAs) is lost. Taken together, our results suggest that Spt6 is required for multiple steps in heterochromatic silencing by controlling chromatin, transcriptional, and post-transcriptional processes.

2011-10-20 | E-MTAB-738 | biostudies-arrayexpress

High-througput sequencing of the rtel1 mutant

Project description:RNA sequencing performed on the root tips of rtel1 mutants and Col-0

2016-09-01 | E-MTAB-2943 | biostudies-arrayexpress

Nucleosome remodeler exclusion by histone deacetylation enforces heterochromatic silencing and epigenetic inheritance

Project description:Heterochromatin enforces transcriptional gene silencing and can be epigenetically inherited, but the underlying mechanism has remained unclear.Here we show that histone deacetylation, a conserved feature of heterochromatin domains, blocks SWI/SNF subfamily remodelers involved in chromatin unraveling, thereby stabilizing modified nucleosomes that preserve gene silencing. Histone hyperacetylation, resulting from either the loss of a histone deacetylase (HDAC) or the direct targeting of histone acetyltransferase to heterochromatin, permits remodeler access, leading to silencing defects.The requirement for HDAC in heterochromatin silencing can be bypassedby impeding SWI/SNF activity. Highlighting the crucial role of remodelers, merely targeting SWI/SNF to heterochromatin, even in cells with functional HDAC, increases nucleosome turnover, causing defective gene silencing and compromised epigenetic inheritance. This study elucidates a fundamental mechanism whereby histone hypoacetylation, maintained by high HDAC levels in heterochromatic regions, ensures stable gene silencing and epigenetic inheritance,providing significant insights into genome regulation relevant to human diseases.

2024-08-05 | GSE269243 | GEO

Nucleosome remodeler exclusion by histone deacetylation enforces heterochromatic silencing and epigenetic inheritance

Project description:Nucleosome remodeler exclusion by histone deacetylation enforces heterochromatic silencing and epigenetic inheritance

| PRJNA1120798 | ENA

Comparative genome-wide transcriptional profile after RTEL1 depletion and G4 stabilisation.

Project description:The goal of this study is to compare the transcription profile of mouse embryonic fibroblasts upon deletion of the helicase RTEL1 and stabilisation of G-quadruplexes (G4) with the G4 stabilisation drug TMPyP4.

2021-01-04 | GSE149850 | GEO

Clr4SUV39H1 ubiquitination and non-coding RNA mediate transcriptional silencing via heterochromatic phase transitions

Project description:Clr4SUV39H1 ubiquitination and non-coding RNA mediate transcriptional silencing via heterochromatic phase transitions

| PRJNA656575 | ENA

SMARCA4 Phosphorilation inhibition

Project description:Cyclin-Dependent Kinase 9 (CDK9) as part of the PTEFb complex promotes transcriptional elongation and high-level gene expression. We now report that, paradoxically, CDK9 is also essential for maintaining gene silencing at heterochromatic loci. Through a live cell screen, we discovered that CDK9 inhibition reactivates epigenetically silenced genes in cancer, leading to restored tumor suppressor gene expression and cell differentiation, along with activation of endogenous retrovirus (ERV) genes. CDK9 inhibition maintains gene silencing directly through phosphorylation of the SWI/SNF protein SMARCA4 and indirectly through HP1α activation. Based on gene activation, we developed the highly selective and 2 potent CDK9 inhibitor MC180295 (IC50 =5.1nM) that has broad anti-cancer activity in-vitro and is effective in in-vivo cancer models. Additionally, CDK9 inhibition synergizes with the immune checkpoint inhibitor α-PD-1 in vivo, making it an excellent target for epigenetic therapy of cancer.

2023-06-13 | PXD008040 | Pride

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