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M6A RNA methylation of major satellite repeat transcripts facilitates chromatin association and RNA:DNA hybrid formation in mouse heterochromatin

ABSTRACT: m6A RNA methylation of major satellite repeat transcripts facilitates chromatin association and RNA:DNA hybrid formation in mouse heterochromatin

PROVIDER: PRJNA658095 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12476683_1.fastq.gz	Fastqsanger.gz
	SRR12476683_2.fastq.gz	Fastqsanger.gz
	SRR12476684_1.fastq.gz	Fastqsanger.gz
	SRR12476684_2.fastq.gz	Fastqsanger.gz
	SRR12476685_1.fastq.gz	Fastqsanger.gz

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m6A RNA methylation of major satellite repeat transcripts facilitates chromatin association and RNA:DNA hybrid formation in mouse heterochromatin

Project description:m6A RNA methylation of major satellite repeat transcripts facilitates chromatin association and RNA:DNA hybrid formation in mouse heterochromatin

2021-04-21 | GSE156481 | GEO

The isoflavone genistein selectively derepresses major satellite repeat transcription in mouse heterochromatin

Project description:Heterochromatin has crucial functions in protecting genome integrity. In mouse cells, heterochromatin is characterized by A/T-rich, 234 bp DNA repeat arrays, called the major satellite repeats (MSR). We investigated MSR expression in response to a variety of stress conditions by using small molecule compounds. We identified the isoflavone genistein to selectively derepress MSR transcription but not that of other DNA repeat elements. Genistein is a natural compound that is frequently used in dietary supplements and has been associated with reducing cancer risk. A 24 hrs exposure of mouse embryonic fibroblasts (MEF) to genistein results in a more than 100-fold induction of MSR transcripts. This derepression depends on the activity of RNA polymerase II and requires a cycling G1 cell population. Blocking the cell cycle at the G2/M stage significantly attenuates genistein- mediated derepression of MSR transcription. Mechanistically, DNA topoisomerase poisons phenocopy the genistein-dependent desilencing of MSR expression. Together, these data suggest that MSR transcriptional response is guided by an altered topology of the underlying A/T-rich MSR DNA repeat arrays. In addition, the data reveal a novel function for genistein in derepressing MSR transcription that may contribute to the growth inhibitory and anticancer properties of this natural compound.

2025-09-03 | GSE291747 | GEO

Forced expression of MSR repeat transcripts breaks heterochromatin organization

Project description:Mouse heterochromatin is characterized by transcriptionally competent major satellite repeat (MSR) sequences and it has been proposed that MSR repeat RNA contributes to the integrity of heterochromatin. We established an inducible dCas9-effector system in mouse embryonic fibroblasts, where we can target dCas9-VPR (transcriptional activator) and dCas9-KM (transcriptional repressor) to MSR repeat sequences. We show that induction of dCas9-VPR forces significant MSR RNA output, while induction of dCas9-KM silences MSR transcription. Both approaches perturb heterochromatin organization, where the dCas9-VPR leads to an immediate dispersion of heterochromatin and dCas9-KM induction results in a delayed aggregation of heterochromatin. MEF cells with the forced expression of MSR RNA are not viable and the defects in heterochromatin organization cannot be reverted. This study highlights the importance of restricting MSR RNA output to maintain heterochromatin integrity and also reveals that the structural organization of heterochromatin is governed by the transcriptional state of the underlying MSR repeats.

2025-03-23 | GSE262294 | GEO

The isoflavone genistein selectively derepresses major satellite repeat transcription in mouse heterochromatin [Top2beta]

2025-09-03 | GSE291959 | GEO

The isoflavone genistein selectively derepresses major satellite repeat transcription in mouse heterochromatin

Project description:The isoflavone genistein selectively derepresses major satellite repeat transcription in mouse heterochromatin

| PRJNA1235182 | ENA

m6A RNA methylation of major satellite repeat transcripts facilitates chromatin association and RNA:DNA hybrid formation in mouse heterochromatin.

Project description:Heterochromatin has essential functions in maintaining chromosome structure, in protecting genome integrity and in stabilizing gene expression programs. Heterochromatin is often nucleated by underlying DNA repeat sequences, such as major satellite repeats (MSR) and long interspersed nuclear elements (LINE). In order to establish heterochromatin, MSR and LINE elements need to be transcriptionally competent and generate non-coding repeat RNA that remain chromatin associated. We explored whether these heterochromatic RNA, similar to DNA and histones, may be methylated, particularly for 5-methylcytosine (5mC) or methyl-6-adenosine (m6A). Our analysis in mouse ES cells identifies only background level of 5mC but significant enrichment for m6A on heterochromatic RNA. Moreover, MSR transcripts are a novel target for m6A RNA modification, and their m6A RNA enrichment is decreased in ES cells that are mutant for Mettl3 or Mettl14, which encode components of a central RNA methyltransferase complex. Importantly, MSR transcripts that are partially deficient in m6A RNA methylation display impaired chromatin association and have a reduced potential to form RNA:DNA hybrids. We propose that m6A modification of MSR RNA will enhance the functions of MSR repeat transcripts to stabilize mouse heterochromatin.

| S-EPMC8191757 | biostudies-literature

The isoflavone genistein selectively derepresses major satellite repeat transcription in mouse heterochromatin [Top2beta]

Project description:The isoflavone genistein selectively derepresses major satellite repeat transcription in mouse heterochromatin [Top2beta]

| PRJNA1236257 | ENA

Major satellite repeat RNA stabilize heterochromatin retention of Suv39h enzymes by RNA-nucleosome association and RNA:DNA hybrid formation

Project description:Molecular definition of an RNA-mediated mechanism that stabilizes association of the Suv39h enzymes at mouse heterochromatin.

2017-08-03 | GSE100222 | GEO

The Nuclear Matrix Protein SAFB Cooperates with Major Satellite RNAs to Stabilize Heterochromatin Architecture Partially through Phase Separation [RNA-seq]

Project description:Interphase chromatin is hierarchically organized into higher-order architectures that are essential for gene functions, yet the biomolecules that regulate these 3D architectures remain poorly understood. Here, we show that scaffold attachment factor B (SAFB), a nuclear matrix (NM)-associated protein with RNA- binding functions, modulates chromatin condensa- tion and stabilizes heterochromatin foci in mouse cells. SAFB interacts via its R/G-rich region with heterochromatin-associated repeat transcripts such as major satellite RNAs, which promote the phase separation driven by SAFB. Depletion of SAFB leads to changes in 3D genome organization, including an increase in interchromosomal interactions adjacent to pericentromeric heterochromatin and a decrease in genomic compartmentalization, which could result from the decondensation of pericentromeric heterochromatin. Collectively, we reveal the integrated roles of NM-associated proteins and repeat RNAs in the 3D organization of heterochromatin, which may shed light on the molecular mechanisms of nuclear architecture organization.

2019-12-03 | GSE141294 | GEO

Forced expression of MSR repeat transcripts above a threshold limit breaks heterochromatin organization

Project description:Mouse heterochromatin is characterised by transcriptionally competent major satellite repeat (MSR) sequences and it has been proposed that MSR RNA contributes to the integrity of heterochromatin. We established an inducible dCas9-effector system in mouse embryonic fibroblasts, where we can modulate MSR transcription through the targeting of a dCas9-Repressor or a dCas9-Activator. With this system, we can define a threshold limit of >300-fold deregulation of MSR transcript levels, above which the structural organisation of heterochromatin becomes disrupted. MEF cells expressing MSR RNA above this threshold limit are not viable and the defects in heterochromatin organisation and chromosome segregation cannot be reverted. This study highlights the importance of restricting MSR RNA output to maintain heterochromatin integrity and relates MSR transcript levels to either physiological or pathological conditions. It also reveals that the structural organisation of heterochromatin is governed by the transcriptional chromatin state and associated MSR RNA of the MSR repeats.

2025-06-05 | GSE287837 | GEO

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