The ontogeny of X-chromosome inactivation in the mouse: two current views
(A) The de novo inactivation model requires many rounds of inactivation and reactivation: the paternal germline initiates meiotic sex-chromosome inactivation, but the X chromosome is completely reactivated after meiosis. The zygote inherits two fully active X chromosomes and begins re-inactivation of the paternal X chromosome (XP) at the 4- to 8-cell stage. In the trophectoderm (extra-embryonic cells, shown in blue), XP silencing is maintained, therefore accounting for the imprinted form of X-chromosome inactivation. By contrast, in the epiblast (green cells), yet another round of reactivation takes place in preparation for a final round of inactivation in the form of random X-chromosome inactivation. (B) In the pre-inactivation model, the female zygote inherits a partially silent XP and maintains the silent state throughout pre-implantation development. Silencing becomes globalized and complete in extra-embryonic tissues. This accounts for the imprinted form of X-chromosome inactivation. By contrast, the epiblast cells of the inner cell mass (ICM) undergo a single round of reactivation followed by a random form of X-chromosome inactivation.
This image is linked to the following Scitable pages:
Females (XX) carry twice as many X-linked genes on their sex chromosomes as males (XY). How do cells control gene expression to manage this potentially lethal dosage problem?
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