Karen Ng*, Dieter Pullirsch*, Martin Leeb* & Anton Wutz
Research Institute of Molecular Pathology, Dr Bohr-Gasse 7, 1030 Vienna, Austria
To whom correspondence should be addressed
Anton Wutz Tel: +43 1 79730 521; Fax: +43 1 7987 153;
wutz@imp.univie.ac.at
* These authors contributed equally to this work
Received 26 June 2006; Accepted 6 November 2006.
Abstract
X inactivation is the mechanism by which mammals adjust the genetic imbalance that arises from the different numbers of gene-rich X-chromosomes between the sexes. The dosage difference between XX females and XY males is functionally equalized by silencing one of the two X chromosomes in females. This dosage-compensation mechanism seems to have arisen concurrently with early mammalian evolution and is based on the long functional Xist RNA, which is unique to placental mammals. It is likely that previously existing mechanisms for other cellular functions have been recruited and adapted for the evolution of X inactivation. Here, we critically review our understanding of dosage compensation in placental mammals and place these findings in the context of other cellular processes that intersect with mammalian dosage compensation.
