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. 2017 Nov 3;8:1297. doi: 10.1038/s41467-017-01415-5

Fig. 6.

Fig. 6

Representation of Xp reactivation and different X-linked gene behaviours. Scheme of imprinted XCI, followed by reactivation in the ICM of the blastocyst. Xp silencing is triggered by the long non-coding Xist RNA, followed by H3K27me3 recruitment. At the early blastocyst stage (E3.5), imprinted Xp is maintained in TE, when some genes are already showing reactivation in the ICM, independently of Xist (early-reactivated genes). Those early genes are lowly enriched in H3K27me3 marks and highly enriched in H3K4me3 on their paternal allele compared to the later reactivated ones. A few hours later, when ICM cells are divided into PrE and Epi cells, Xp reactivation appears to be nearly complete only in the future epiblast cells, (based on loss of Xist coating and H3K27me3). In PrE, some early-reactivated genes have already been silenced again. This suggests a fluctuation of early-reactivated genes with different epigenetic memory requirements between early- and late-reactivated genes. TE trophectoderm, PrE primitive endoderm, ICM inner cell mass, Epi epiblast