ArticleInternational journal of molecular sciences2017
The Regulatory Capacity of Bivalent Genes-A Theoretical Approach.
Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Stochastic modeling of epigenetic memory.NPJ systems biology and applications · 2026Review
- Organoid Cultures In Silico: Tools or Toys?Bioengineering (Basel, Switzerland) · 2022Review
- Epigenetic factor competition reshapes the EMT landscape.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Article
- Bivalent chromatin as a therapeutic target in cancer: An in silico predictive approach for combining epigenetic drugs.PLoS computational biology · 2021Article
- Loss of EZH2-like or SU(VAR)3-9-like proteins causes simultaneous perturbations in H3K27 and H3K9 tri-methylation and associated developmental defects in the fungus Podospora anserina.Epigenetics & chromatin · 2021Article
- Genome-Wide Histone Modifications and CTCF Enrichment Predict Gene Expression in Sheep Macrophages.Frontiers in genetics · 2020Article
- Article
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Authors and funding
4 authors.
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Abstract
Bivalent genes are frequently associated with developmental and lineage specification processes. Resolving their bivalency enables fast changes in their expression, which potentially can trigger cell fate decisions. Here, we provide a theoretical model of bivalency that allows for predictions on the occurrence, stability and regulatory capacity of this prominent modification state. We suggest that bivalency enables balanced gene expression heterogeneity that constitutes a prerequisite of robust lineage priming in somatic stem cells. Moreover, we demonstrate that interactions between the histone and DNA methylation machineries together with the proliferation activity control the stability of the bivalent state and can turn it into an unmodified state. We suggest that deregulation of these interactions underlies cell transformation processes as associated with acute myeloid leukemia (AML) and provide a model of AML blast formation following deregulation of the Ten-eleven Translocation (TET) pathway.
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Registered trials
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