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Origin of Cellular Asymmetries in the Pre-Implantation Mouse Embryo: A Hypothesis


Origin of Cellular Asymmetries in the Pre-Implantation Mouse Embryo: A Hypothesis

Katsuyoshi Takaoka et al. Philos Trans R Soc Lond B Biol Sci.


The first cell fate decision during mouse development concerns whether a blastomere will contribute to the inner cell mass (ICM; which gives rise to the embryo proper) or to trophectoderm (TE; which gives rise to the placenta). The position of a cell within an 8- to 16-cell-stage embryo correlates with its future fate, with outer cells contributing to TE and inner cells to the ICM. It remains unknown, however, whether an earlier pre-pattern exists. Here, we propose a hypothesis that could account for generation of such a pre-pattern and which is based on epigenetic asymmetry (such as in histone or DNA methylation) between maternal and paternal genomes in the zygote.

Keywords: cell fate; epigenetic; mouse embryo; pre-implantation.


Figure 1.
Figure 1.
Hypothetical model for generation of an early embryonic pre-pattern based on epigenetic asymmetry between parental genomes. The maternal (M) genome and its derivatives are shown in orange, whereas the paternal (P) genome and its derivatives are shown in blue. Asymmetric modification of parental genomes (either DNA modification or histone modification) is represented by red dots on the maternal chromosome. In this model, asymmetric modification is not inherited by a daughter chromosome after cell division. At the 4-cell stage, de novo modification (black dots) occurs equally on maternally and paternally derived genomes. Given that zygotic transcription begins at the 2-cell stage, cells with the maternally derived modification (red dots) at the 2- and 4-cell stages express unknown regulatory genes (green) that will influence the outer–inner position and ICM–TE fate decision at later stages. The second cell from the top at the 4-cell stage contains a low level of the gene products (light green) inherited from its mother cell, which may be sufficient to express regulatory genes. (Online version in colour.)

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