Abstract
During primordial germ cell (PGC) development, epigenetic reprogramming events represented by X chromosome reactivation and erasure of genomic imprinting are known to occur. Although precise timing is not given, X reactivation is thought to take place over a short period of time just before initiation of meiosis. Here, we show that the cessation of Xist expression commences in nascent PGCs, and re-expression of some X-linked genes begins in newly formed PGCs. The X reactivation process was not complete in E14.5 PGCs, indicating that X reactivation in developing PGCs occurs over a prolonged period. These results set the reactivation timing much earlier than previously thought and suggest that X reactivation may involve slow passive steps.
Highlights
In mice, germ cell formation is first observed in postimplantation embryos; primordial germ cells (PGCs) appear at the base of allantois by embryonic day (E) 7.25 [1]
Reactivation just after fertilization has been suggested. These findings indicate that reactivation of the inactive X chromosome occurs at least twice during mammalian development, once in the epiblast cell lineage at the periimplantation stage and once in the PGCs at the midgestation stage, and that the reactivation of the inactive X chromosome appears to be tightly correlated with major genomic reprogramming events occurring during mammalian development [25]
Elucidation of the X reactivation kinetics is important for understanding the mechanism of X chromosome inactivation/reactivation processes and the epigenetic reprogramming processes as well
Summary
Germ cell formation is first observed in postimplantation embryos; primordial germ cells (PGCs) appear at the base of allantois by embryonic day (E) 7.25 [1]. One of two X chromosomes in every cell is inactivated during early embryonic development to compensate gene dosage difference between XY males and XX females [4]. This phenomenon, X chromosome inactivation, represents one of the most remarkable examples of epigenetic gene regulation in mammals. X chromosome inactivation is regulated by a noncoding Xist RNA. Its mechanistic role in gene silencing is not precisely known, the Xist RNA seems to be required for spreading the inactive state along the chromosome. The expression of Xist RNA is negatively regulated by Tsix, the antisense transcript of Xist [11,12]
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