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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens Drosophila melanogaster

PROVIDER: GSE185930 | GEO | 2022/05/23

REPOSITORIES: GEO

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

Project description:Precise control of gene expression underpins normal development. This relies on mechanisms that enable communication between gene promoters and other regulatory elements. In embryonic stem cells (ESCs), the cyclin-dependent kinase module Mediator complex (CKM-Mediator) has been reported to physically link gene regulatory elements to enable gene expression and also prime genes for induction during differentiation. Here, we show that CKM-Mediator contributes little to three-dimensional genome organization in ESCs, but it has a specific and essential role in controlling interactions between inactive gene regulatory elements bound by Polycomb repressive complexes (PRCs). These interactions are established by the canonical PRC1 (cPRC1) complex but rely on CKM-Mediator, which facilitates binding of cPRC1 to its target sites. Importantly, through separation-of-function experiments, we reveal that this collaboration between CKM-Mediator and cPRC1 in creating long-range interactions does not function to prime genes for induction during differentiation. Instead, we discover that priming relies on an interaction-independent mechanism whereby the CKM supports core Mediator engagement with gene promoters during differentiation to enable gene activation.

| S-EPMC9568430 | biostudies-literature

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)

2022-05-23 | GSE185929 | GEO

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

2022-05-23 | GSE185927 | GEO

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

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

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

| PRJNA771378 | ENA

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)

| PRJNA771384 | ENA

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)

| PRJNA771383 | ENA

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

2024-01-03 | GSE188551 | GEO

Inheritance of Polycomb-dependent chromosomal interactions in Drosophila.

Project description:Maintenance of cell identity is a complex task that involves multiple layers of regulation, acting at all levels of chromatin packaging, from nucleosomes to folding of chromosomal domains in the cell nucleus. Polycomb-group (PcG) and trithorax-group (trxG) proteins maintain memory of chromatin states through binding at cis-regulatory elements named PcG response elements or cellular memory modules. Fab-7 is a well-defined cellular memory module involved in regulation of the homeotic gene Abdominal-B (Abd-B). In addition to its action in cis, we show here by three-dimensional FISH that the Fab-7 element leads to association of transgenes with each other or with the endogenous Fab-7, even when inserted in different chromosomes. These long-distance interactions enhance PcG-mediated silencing. They depend on PcG proteins, on DNA sequence homology, and on developmental progression. Once long-distance pairing is abolished by removal of the endogenous Fab-7, the derepressed chromatin state induced at the transgene locus can be transmitted through meiosis into a large fraction of the progeny, even after reintroduction of the endogenous Fab-7. Strikingly, meiotic inheritance of the derepressed state involves loss of pairing between endogenous and transgenic Fab-7. This suggests that transmission of nuclear architecture through cell division might contribute to inheritance of chromatin states in eukaryotes.

| S-EPMC218078 | biostudies-literature

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