Authors
Degen, E. A., Blythe, S. A.
Abstract
Eukaryotic organisms rely on post-translational modifications to chromatin to maintain stable patterns of gene silencing. These modifications include trimethylation at histone H3 lysine 27 (H3K27me3), which is deposited by Polycomb Repressive Complex 2 (PRC2) and accumulates on the genome during embryogenesis. While this process underlies the proper specification of cell types, we lack the ability to quantitatively predict the de novo establishment of Polycomb states. The kinetics of H3K27 methylation is difficult to quantify in vivo, and further, the network of molecular interactions that influences Polycomb states is complex. Here, leveraging the Drosophila embryonic system, we measure H3K27me3 dynamics with ChIP-seq and extract the rate the modification spreads along chromatin in vivo. To provide a mechanistic explanation for this rate, we build a reaction-diffusion framework that models how PRC2 establishes states of gene silencing de novo. The reaction-diffusion system recapitulates experimental observations in wild-type and mutant embryos, and suggests that PRC2 can diffuse in 1D along chromatin at a rate enhanced by Polycomb Repressive Complex 1. Through this work, we define a minimal set of parameters that dictate in vivo Polycomb dynamics, and provide evidence that the early embryo creates a super-charged environment for epigenetic modification.
Preprint server:
bioRxiv
The authors list and abstract were imported from bioRxiv on 28 Aug 2026.
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