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

A long noncoding RNA uses viral mimicry to achieve developmental gene silencing across a chromosome.

Prospective, cross-sectional, and intra-twin study designs identify skewed X chromosome inactivation is associated with cardiovascular disease risk and future cancer diagnosis in the TwinsUK population cohort.

Activity-dependent genetic labeling during behavioral learning shows Fragile-X syndrome model mice exhibit impaired hippocampal engram reactivation, and that enriched environment experience improves fear memory retrieval by enhancing engram reactivation efficacy.

Two complexes that contain the histone acetyl transferase MOF engage in a two-pronged approach to ensure the repression of X inactivation in mouse embryonic stem cells.

Ignoring the probability of species variation when reporting observations about biological processes leads to misinterpretation of the experimental data.

Single embryo RNA-seq combined with mouse genetics provides a comprehensive view on the roles of Rlim and Xist for the regulation of X-linked gene expression during early mouse embryogenesis.

The X-linked loci Firre and Dxz4 are involved in autosomal gene regulation rather than XCI biology.

YTHDC1 is an essential factor controlling satellite cell regenerative ability through multifaceted gene regulatory mechanisms in myoblast cells.

The structure of a voltage-activated potassium channel in lipid nanodiscs solved using cryo-electron microscopy is similar to previous X-ray structures, and provides insights into the mechanism of C-type inactivation.