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Forced expression of MSR repeat transcripts breaks heterochromatin organization

ABSTRACT: Forced expression of MSR repeat transcripts breaks heterochromatin organization

PROVIDER: PRJNA1091166 | ENA |

REPOSITORIES: ENA

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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.

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mRNA expression profile of A549 cells and MSR-A549 cells with or without JQ1 treatment

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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

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Genome-wide maps of histone H3K27 acetylation in A549 and MSR-A549 cells.

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Satellite repeat transcripts modulate heterochromatin condensates and safeguard chromosome stability in mouse embryonic stem cells.

Project description:Heterochromatin maintains genome integrity and function, and is organised into distinct nuclear domains. Some of these domains are proposed to form by phase separation through the accumulation of HP1ɑ. Mouse heterochromatin contains noncoding major satellite repeats (MSR), which are highly transcribed in mouse embryonic stem cells (ESCs). Here, we report that MSR transcripts can drive the formation of HP1ɑ droplets in vitro, and modulate heterochromatin into dynamic condensates in ESCs, contributing to the formation of large nuclear domains that are characteristic of pluripotent cells. Depleting MSR transcripts causes heterochromatin to transition into a more compact and static state. Unexpectedly, changing heterochromatin's biophysical properties has severe consequences for ESCs, including chromosome instability and mitotic defects. These findings uncover an essential role for MSR transcripts in modulating the organisation and properties of heterochromatin to preserve genome stability. They also provide insights into the processes that could regulate phase separation and the functional consequences of disrupting the properties of heterochromatin condensates.

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DOT1L regulates pericentromeric heterochromatin

Project description:Many repetitive DNA elements are packaged in heterochromatin, but depend on occasional transcription to maintain long-term silencing. The factors that promote transcription of repeat elements in heterochromatin are largely unknown. Here, we show that DOT1L, a histone methyltransferase that modifies lysine 79 of histone H3 (H3K79), is required for transcription of major satellite repeats to maintain pericentromeric heterochromatin (PCH), and that this function is essential for preimplantation development. DOT1L is a transcriptional activator at single-copy genes but does not have a known role in repeat element transcription. We show that H3K79me3 is specifically enriched at repetitive elements, that loss of DOT1L compromises pericentromeric major satellite transcription, and that this function depends on interaction between DOT1L and the chromatin remodeler SMARCA5. DOT1L inhibition causes chromosome breaks and cell cycle defects, and leads to embryonic lethality. Together, our findings uncover a vital new role for DOT1L in transcriptional activation of heterochromatic repeats.

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RNA-RNA interaction analysis of functional SINE repeat elements-derived transcripts

Project description:We studied functional and structural features of mouse and human SINE repeat elements-derived RNAs in SINEUP long non-coding RNAs which upregulate the translation of the target protein coding gene. To check the interaction of functional SINE RNAs with ribosomal RNAs, we created PARIS2 (psoralen analysis of RNA interactions and structures) libraries from SINEUP (with embedded mouse SINEB2 or human FRAM repeat) and the target sense GFP plasmids co-transfected human cells.

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