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DNA methylation shapes the Polycomb landscape during the exit from naive pluripotency
Julien Richard Albert1, Teresa Urli1, Ana Monteagudo-Sánchez1,2
1Université Paris Cité, CNRS, Institut Jacques Monod, Paris, France.
Nature Structural & Molecular Biology
|October 25, 2024
Summary
DNA methylation (5mC) and H3K27me3 are antagonistic epigenetic marks. 5mC can directly restrict H3K27me3, promoting gene activation and impacting development and cancer.
Area of Science:
- Epigenetics
- Developmental Biology
- Cancer Biology
Background:
- 5-methylcytosine (5mC) and histone 3 lysine 27 trimethylation (H3K27me3) are generally mutually exclusive in mammals.
- During mouse embryonic stem cell differentiation, 5mC increases while H3K27me3 is restricted to specific regions.
Purpose of the Study:
- To investigate how 5mC influences the H3K27me3 landscape.
- To determine the role of DNA methylation machinery in H3K27me3 restriction.
Main Methods:
- Epigenome profiling of naive and differentiated cells with and without DNA methylation machinery.
- Site-directed epigenome editing to modulate 5mC levels.
- Analysis of gene expression changes.
Main Results:
- 5mC accumulation is not the primary driver for restricting most H3K27me3 domains; aberrant Ezhip expression mediates this.
- At specific regions, 5mC deposition directly antagonizes H3K27me3, leading to gene activation.
- 163 candidate genes were identified that require 5mC or H3K27me3 depletion for activation.
Conclusions:
- H3K27me3 restriction is influenced by 5mC both directly and indirectly.
- 5mC plays a noncanonical role in gene activation, relevant to development and cancer progression.
- Dynamic replacement of 5mC and H3K27me3 is observed in oncogenic cells.
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