ArticleNature structural & molecular biology2022
Distinct roles for CKM-Mediator in controlling Polycomb-dependent chromosomal interactions and priming genes for induction.
Article in Nature structural & molecular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- Mechanisms and functional implications of long-range enhancer-dependent gene regulation.Nature genetics · 2026Review
- Article
- Polycomb-mediated 3D chromatin interactions in gene regulation.Current opinion in genetics & development · 2026Review
- Transient histone deacetylase inhibition induces cellular memory of gene expression and 3D genome folding.Nature genetics · 2026Article
- Enhancer-dependent gene regulation in space, time, and malignancies.International journal of cancer · 2026Review
- 3D genome folding in epigenetic regulation and cellular memory.Trends in cell biology · 2026Review
- Article
- Engineering the Link: From Genome Interaction Maps to Functional Insight.Advanced biology · 2025Review
- A semidominant point mutation of Mediator tail subunit MED5b in Arabidopsis leads to altered enrichment of H3K27me3 and reduced expression of targets of MYC2.G3 (Bethesda, Md.) · 2025Article
- Structural basis of the human transcriptional Mediator regulated by its dissociable kinase module.Molecular cell · 2024Article
- Structures and compositional dynamics of Mediator in transcription regulation.Current opinion in structural biology · 2024Review
- The Wild West of spike-in normalization.Nature biotechnology · 2024Article
- Attraction and disruption: how loop extrusion and compartmentalisation shape the nuclear genome.Current opinion in genetics & development · 2024Review
- Crosstalk within and beyond the Polycomb repressive system.The Journal of cell biology · 2024Review
- YY1 binding is a gene-intrinsic barrier to Xist-mediated gene silencing.EMBO reports · 2024Article
- MLL-AF4 cooperates with PAF1 and FACT to drive high-density enhancer interactions in leukemia.Nature communications · 2023Article
- Ultra-long-range interactions between active regulatory elements.Genome research · 2023Article
- Changes in PRC1 activity during interphase modulate lineage transition in pluripotent cells.Nature communications · 2023Article
- RINGs, DUBs and Abnormal Brain Growth-Histone H2A Ubiquitination in Brain Development and Disease.Epigenomes · 2022Review
- Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.