One of the two X chromosomes in female cells randomly becomes inactive throughout development. When the Xist genes transcribed RNA covers the whole X chromosome on the X chromosome from which it is produced, inactivation takes place. Nesterova and colleagues examine the function of the RNA interference pathway enzyme Dicer in the DNA methylation of the Xist promoter in the inaugural issue of Epigenetics and Chromatin. In order to equalise the dosage of X chromosome gene products between XX females and XY men, one X chromosome must be transcriptionally silenced in female mammalian cells. Early in development, the X chromosome becomes inactive in the embryo (Edem et al., 2012). Equal chances exist for both X chromosomes to be silenced. Once established, silencing is enduring because the identical X chromosome stays inactive in all succeeding cell generations. As a result, each female is made up of a mosaic of cells in which the X gene from either the mother or the father is silenced. In the first issue of Epigenetics and Chromatin, Nesterova and colleagues provide new insight into the regulation of this process. In order to equalise the amounts of X-linked gene expression across the sexes in mammalian female cells, X-chromosome inactivation (XCI) is one type of dosage compensation. Due to inactivation escape and skewing, XCI is linked to a variety of disorders, and the severity of these diseases also heavily depends on the state of XCI. Three categories may be made of them: X-linked disorders, XCI escaperelated illnesses, and X-chromosome aneuploidy. Here, we evaluate representative illnesses in terms of their description, signs, and symptoms, as well as XCI's part in their aetiology (Haratym 2002)
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