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.

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

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.

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.

Chromatin profiling of Drosophila testes reveals activation of the transcriptional program of the germline, widespread changes in RNA polymerase progression, and the absence of chromosomal regulation across the X chromosome.

N‑terminus of MSL1 protein, involved in dosage compensation in Drosophila, is required for the interaction with non-coding roX2 RNA and the assembly of the complex on the male X chromosome.

Allele-specific expression due to genetic differences, X-chromosome inactivation or genomic imprinting, varies dynamically throughout development, and may be explained by allele-specific differences in stability or the actions of tissue-specific enhancers.