The accompanying photograph seems at first glance to capture a straightforward fluorescence in situ hybridization experiment, with each colored dot representing a tagged probe bound to a particular locus. But the details of the data tell an intriguing story. The image is taken from findings presented on page 339 by Nandita Singh and colleagues showing that chromosome-pair non-equivalence is not limited to the specific instances of imprinting and X-chromosome inactivation but may be much more widespread, at least in the mouse genome.

The results of Singh et al. are part of a line of work on the replication timing of a group of genes that are expressed mono-allelically in a random manner (genes that are expressed from either the paternal or maternal chromosome, with variation from cell to cell). Such genes are represented in several gene families, including odorant receptors and T-cell receptors. Whereas most genes are replicated synchronously, monoallelically expressed genes are asynchronously replicated in S phase. As these genes are scattered throughout the genome, Singh and colleagues asked whether the observed asynchronous replication was coordinated in any way.

The answer is found in this picture and in others like it. In this particular mouse embryonic fibroblast, the red dot corresponds to the odorant-receptor gene Olfr1 and the green dot to the odorant-receptor gene Olfr10, which are 14 cM apart on chromosome 11. The linked double-dot signals on the left indicate that the early-replicating allele for each gene is on the same chromosome. Notably, this coordination holds true for several monoallelically expressed loci on chromosomes 2, 6 and 7 as well, and is not limited to odorant-receptor genes.

That these loci are distant from each other along a chromosome, with many intervening genes that replicate synchronously, suggests some kind of 'spooky action at a distance,' to borrow a phrase from quantum mechanics. Although the coordinated replication of these scattered alleles is in some ways more perplexing than whole-chromosome X inactivation, the authors suggest that similar mechanisms may be involved.