Peter W. Lewis

This study identifies EZH2 serine 21 phosphorylation as a mechanism that limits PRC2 activation and H3K27me3 propagation, affecting developmental processes in mesenchymal progenitor cells.

This study identifies that both sequence-specific DNA binding and disordered protein domains are required for pioneer-factor chromatin occupancy, with mitotic retention relying only on DNA binding.

The paper identifies distinct DAXX effector modules that separate H3.3 nucleosome assembly from ERV silencing, showing H3.3 is dispensable for repression but SUMO-dependent recruitment is required.

The paper identifies SUZ12's nucleic acid-binding domain as critical for regulating PRC2 activity in H3 K27M gliomas, showing how it constrains enzymatic function and maintains targeted gene silencing.

The paper identifies chromatin regulators that modify developmental defects caused by PRC2 inhibition in Drosophila, revealing pathways that restore normal development despite disrupted H3K27me3.

This study identifies a second HuSH complex, HuSH2, and shows its role in LINE-1 element silencing through interactions with MPP8 and expression dynamics.

This study re-evaluates the bivalency model using a new ChIP method, finding widespread bivalency that does not resolve with differentiation and is not specific for poised developmental genes.