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.

Chromosome segregation in male spermatocytes exhibits anaphase A without shortening of autosome-associated microtubules and partitioning of an unpaired X chromosome that is initiated by an imbalance of attached kinetochore microtubules.

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.

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.

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.

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.

Loading and linear translocation of condensin dosage compensation along the X-chromosomes create the loop-anchored topologically associating domains detected by Hi-C.

Many different human cell lines, including both normal and cancer cells, appear to converge to a state that contains an unusual number of chromosomes when they are grown in culture.

An analysis of gene dosage at the DNA, RNA and protein level yields new insights into the early stages of Z-chromosome dosage compensation in schistosome parasites.

A paternal bias in germline mutation is seen throughout amniotes and may be explained by sex differences in DNA damage and repair after primordial germ cell specification.