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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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			Action	DRS
	SRR28427100_1.fastq.gz	Fastqsanger.gz
	SRR28427100_2.fastq.gz	Fastqsanger.gz
	SRR28427101_1.fastq.gz	Fastqsanger.gz
	SRR28427101_2.fastq.gz	Fastqsanger.gz
	SRR28427102_1.fastq.gz	Fastqsanger.gz

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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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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.

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