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Distinct roles for CDK-Mediator in controlling Polycomb-dependent chromosomal interactions and priming genes for induction (CaptureC)

ABSTRACT: Distinct roles for CDK-Mediator in controlling Polycomb-dependent chromosomal interactions and priming genes for induction (CaptureC)

PROVIDER: PRJNA771378 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16345010_1.fastq.gz	Fastqsanger.gz
	SRR16345010_2.fastq.gz	Fastqsanger.gz
	SRR16345011_1.fastq.gz	Fastqsanger.gz
	SRR16345011_2.fastq.gz	Fastqsanger.gz
	SRR16345012_1.fastq.gz	Fastqsanger.gz

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Distinct roles for CDK-Mediator in controlling Polycomb-dependent chromosomal interactions and priming genes for induction (CaptureC)

Project description:Precise control of gene expression is essential for normal development. This is thought to rely on mechanisms that enable communication between gene promoters and other regulatory elements. In embryonic stem cells (ESCs) the CDK-Mediator (CDK-MED) complex has been reported to topologically link gene regulatory elements to enable gene expression and also prime genes for induction during differentiation. Here we discover that CDK-MED contributes little to overall genome organisation in ESCs, but interestingly has a specific and essential role in controlling interactions between inactive gene regulatory elements bound by the Polycomb repressive complexes (PRCs). These interactions are facilitated by CDK-MED but rely on canonical PRC1. However, through separation of function experiments, we reveal that the collaboration between CDK-MED and cPRC1 in creating long-range interactions does not function to prime genes for induction during differentiation. Instead, we discover that priming relies on a topology-independent mechanism whereby the CDK module supports core Mediator engagement with gene promoters to support gene activation.

2022-05-23 | GSE185926 | GEO

Distinct roles for CDK-Mediator in controlling Polycomb-dependent chromosomal interactions and priming genes for induction (RNA-Seq)

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Distinct roles for CDK-Mediator in controlling Polycomb-dependent chromosomal interactions and priming genes for induction (ChIP-Seq)

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A dual role for CDK-Mediator in controlling Polycomb-dependent topology and priming genes for induction [Hi-C]

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Distinct roles for CDK-Mediator in controlling Polycomb-dependent chromosomal interactions and priming genes for induction (ChIP-Seq)

Project description:Distinct roles for CDK-Mediator in controlling Polycomb-dependent chromosomal interactions and priming genes for induction (ChIP-Seq)

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Distinct roles for CDK-Mediator in controlling Polycomb-dependent chromosomal interactions and priming genes for induction (RNA-Seq)

Project description:Distinct roles for CDK-Mediator in controlling Polycomb-dependent chromosomal interactions and priming genes for induction (RNA-Seq)

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CDK-Mediator and FBXL19 cooperate in the induction of developmental genes by promoting regulatory interactions [CaptureC]

Project description:CDK-Mediator and FBXL19 cooperate in the induction of developmental genes by promoting regulatory interactions [CaptureC]

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CDK-Mediator and FBXL19 cooperate in the induction of developmental genes by promoting regulatory interactions [CaptureC]

Project description:Appropriate developmental gene regulation relies on the capacity of gene promoters to integrate inputs from distal regulatory elements, yet how this is achieved remains poorly understood. In embryonic stem cells (ESCs), a subset of silent developmental gene promoters are primed for activation by FBXL19, a CpG island binding protein, through its capacity to recruit CDK-Mediator. How mechanistically these proteins function together to prime genes for activation during differentiation is unknown. Here we discover that in mouse ESCs FBXL19 and CDK-Mediator support long-range interactions between silent gene promoters that rely on FBXL19 for their induction during differentiation and gene regulatory elements. During gene induction, these distal regulatory elements behave in an atypical manner, in that the majority do not acquire histone H3 lysine 27 acetylation and no longer interact with their target gene promoter following gene activation. Despite these atypical features, we demonstrate by targeted deletions that these distal elements are required for appropriate gene induction during differentiation. Together these discoveries demonstrate that CpG-island associated gene promoters can prime genes for activation by communicating with atypical distal gene regulatory elements to achieve appropriate gene expression.

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A dual role for CDK-Mediator in controlling Polycomb-dependent topology and priming genes for induction [Hi-C]

Project description:A dual role for CDK-Mediator in controlling Polycomb-dependent topology and priming genes for induction [Hi-C]

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Distinct roles of CKM-Mediator in controlling Polycomb-dependent chromosomal interactions and priming genes for induction

Project description:Distinct roles of CKM-Mediator in controlling Polycomb-dependent chromosomal interactions and priming genes for induction

| PRJNA771381 | ENA