C. elegans equalizes the expression of X-chromosome genes between the sexes by reducing the recruitment of RNA polymerase II to promoters of X-linked genes in hermaphrodites, using a chromosome-restructuring complex called condensin.

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

Gene regulatory elements can target a chromatin regulatory complex to a single chromosome in the genome through hierarchical specification and long distance cooperation.

A chromosome-wide mechanism balances X-linked gene expression between the sexes in C. elegans, but no similar chromosome-wide mechanism balances gene expression between X chromosomes and autosomes.

Regulatory hierarchies controlling sex determination and X-chromosome dosage compensation between closely-related nematode species are conserved, but X-chromosome target specificity for the condensin dosage compensation complex has diverged, thereby contributing to reproductive isolation.

RNA binding protein FOX-1 functions as a dose-dependent X-signal element to communicate X-chromosome number and determine nematode sex by controlling alternative non-productive pre-mRNA splicing of the master sex-determination switch gene.

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.

For the first time in a mosquito species an initial Y chromosome signal has been shown to regulate dosage compensation by increasing X chromosome gene expression.

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

Human cell lines regress to become ‘de-sexualized’ by reconfiguring to a 2:3 X/A ratio of high fitness, thus shedding light on the evolution of mammalian sex chromosomes.