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The PRC2 Polycomb complex made in the mouse oocyte prevents transcriptional inactivation of the maternal X-chromosome in the early embryo.

Increased Notch signaling enhances germ cell reprograming in C. elegans by antagonizing PRC2-mediated repression, which results in the activation of UTX-1 and other reprograming-promoting genes.

Telomeric TRF1 controls the transcriptional programmes of pluripotent stem cells by recruiting PRC2 to pluripotency and differentiation genes by controlling the expression of those gene sites and the binding of TERRA RNAs to them.

Optogenetic experiments show that bridging microtubules buffer chromosome movements and promote their alignment through forces transferred to the associated kinetochore fibers, which rely on precise regulation of the overlap region.

Polycomb repressive complex 1.1 restricts precocious myeloid differentiation of hematopoietic stem/progenitor cells and expansion of myeloid progenitors, thereby serving as a gatekeeper of emergency myelopoiesis and myeloid transformation.

Poised neuronal genes are repressed by REST and Polycomb in embryonic stem cells independently and via different chromatin modifications.

Electron microscopy has been used to produce the first three-dimensional image of the PRC2 gene-silencing complex.

Human cell lines replicate and proliferate without ORC1 or ORC2, two subunits of the replication initiator protein complex ORC, which has till now been considered essential for DNA replication.

Epigenetic drift of H3K27me3 is one of the molecular mechanisms that contribute to aging, and stimulation of glycolysis promotes metabolic health and longevity.

The employment of xenopsin in ciliary and mixed microvillar/ciliary eye sensory cells in several protostome animals suggests high evolutionary plasticity of photoreceptors.