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
| Identifer | oai:union.ndltd.org:DRESDEN/oai:qucosa:de:qucosa:89595 |
| Date | 07 February 2024 |
| Creators | Thalheim, Torsten, Herberg, Maria, Löffler, Markus, Galle, Jörg |
| Publisher | MDPI |
| Source Sets | Hochschulschriftenserver (HSSS) der SLUB Dresden |
| Language | English |
| Detected Language | English |
| Type | info:eu-repo/semantics/publishedVersion, doc-type:article, info:eu-repo/semantics/article, doc-type:Text |
| Rights | info:eu-repo/semantics/openAccess |
| Relation | 1069 |
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