X chromosome inactivation in mammals results in the cis-limited inactivation of most, but not all, genes on one of the two X chromosomes present in normal female somatic cells, thus achieving dosage equivalence with males (Lyon 1961; Beutler et al. 1962). Although the basic features of the original X inactivation hypothesis have been established, the molecular mechanism of inactivation and its developmental and genetic control remain unclear. The events in early development that result in stable transcriptional inactivation of up to thousands of genes in a coordinated fashion exert their influence over enormous molecular distances, but only in cis, as the equivalent loci on the homologous chromosome in the same nucleus remain unaffected. X inactivation thus remains among the most fascinating and long-ranging examples of epigenetic control of gene expression (for review, see Gartler et al. 1992; Brown and Willard 1993; Lyon 1993).
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Willard et al. (1993) studied this question.