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Xist-seeded nucleation sites form local concentration gradients of silencing proteins to inactivate the X-chromosome [I]

ABSTRACT: Xist-seeded nucleation sites form local concentration gradients of silencing proteins to inactivate the X-chromosome [I]

PROVIDER: PRJNA680314 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13114388_1.fastq.gz	Fastqsanger.gz
	SRR13114388_2.fastq.gz	Fastqsanger.gz
	SRR13114389_1.fastq.gz	Fastqsanger.gz
	SRR13114389_2.fastq.gz	Fastqsanger.gz
	SRR13114390_1.fastq.gz	Fastqsanger.gz

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Xist-seeded nucleation sites form local concentration gradients of silencing proteins to inactivate the X-chromosome

Project description:Xist-seeded nucleation sites form local concentration gradients of silencing proteins to inactivate the X-chromosome

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Xist-seeded nucleation sites form local concentration gradients of silencing proteins to inactivate the X-chromosome [II]

Project description:Xist-seeded nucleation sites form local concentration gradients of silencing proteins to inactivate the X-chromosome [II]

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Xist-seeded nucleation sites form local concentration gradients of silencing proteins to inactivate the X-chromosome

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2021-10-26 | GSE181236 | GEO

Xist-seeded nucleation sites form local concentration gradients of silencing proteins to inactivate the X-chromosome [II]

Project description:The long non-coding RNA Xist exploits numerous effector proteins to gradually induce gene silencing across the X chromosome. Here, we show that formation of the inactive X (Xi)-compartment is induced by ~50 locally confined granules, where two Xist RNA molecules nucleate supra-molecular complexes (SMCs) of interacting proteins. Xist-SMCs are dynamic structures that concentrate rapidly recycling proteins on the X by increasing their binding affinity, thereby facilitating their access to the entire chromosome. We find that gene silencing originates at Xist-SMCs and propagates across the entire X chromosome over time. The propagation of silencing is achieved by Polycomb-mediated coalescence of chromatin regions and aggregation of the critical silencing enzyme SPEN, via its intrinsically disordered domains. Our observations suggest a new model for X Chromosome Inactivation, whereby Xist RNA triggers macromolecular crowding of heterochromatinizing proteins at distinct sites to ultimately increase their occupancy throughout the X chromosome. This mechanism enables deterministic gene silencing across an entire chromosome without the need for Xist ribonucleoprotein complex-chromatin interactions at each target gene. Our findings uncover a spatial organization mechanism by which few RNA molecules can regulate a broad nuclear compartment through the recruitment and local concentration of dynamic effector proteins, and provide a quantitative framework for studying such compartments.

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Xist-seeded nucleation sites form local concentration gradients of silencing proteins to inactivate the X-chromosome [I]

Project description:The long non-coding RNA Xist exploits numerous effector proteins to gradually induce gene silencing across the X chromosome. Here, we show that formation of the inactive X (Xi)-compartment is induced by ~50 locally confined granules, where two Xist RNA molecules nucleate supra-molecular complexes (SMCs) of interacting proteins. Xist-SMCs are dynamic structures that concentrate rapidly recycling proteins on the X by increasing their binding affinity, thereby facilitating their access to the entire chromosome. We find that gene silencing originates at Xist-SMCs and propagates across the entire X chromosome over time. The propagation of silencing is achieved by Polycomb-mediated coalescence of chromatin regions and aggregation of the critical silencing enzyme SPEN, via its intrinsically disordered domains. Our observations suggest a new model for X Chromosome Inactivation, whereby Xist RNA triggers macromolecular crowding of heterochromatinizing proteins at distinct sites to ultimately increase their occupancy throughout the X chromosome . This mechanism enables deterministic gene silencing across an entire chromosome without the need for Xist ribonucleoprotein complex-chromatin interactions at each target gene. Our findings uncover a spatial organization mechanism by which few RNA molecules can regulate a broad nuclear compartment through the recruitment and local concentration of dynamic effector proteins, and provide a quantitative framework for studying such compartments.

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CIZ1 in Xist seeded assemblies at the inactive X chromosome.

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Project description:Heritable heterochromatin domain formation is initiated by dynamic changes in the proteome on specialized loci, leading to chromatin modifier recruitment, heterochromatin assembly and propagation. Here we characterize the proteomes associated with a defined heterochromatin nucleation region in three distinct chromatin states: before de novo H3K9 methylation nucleation, following heterochromatin assembly and upon heterochromatin disassembly. Our analyses separate sequence-dependent from sequence-independent processes, providing a systematic examination of the template-driven nucleation and epigenetic wiring underlying heterochromatin transmission. We identify functional interactions that reveal an integral role for the conserved nucleolytic Grc3 complex, and its associated network, as pioneer factors in heterochromatin assembly. More broadly, we demonstrate the power of quantitative proteomics-based strategies for the unbiased scrutiny of the single regions assembled in distinct chromatin states.

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