Investigating the role of the early amnion in the guinea pig embryo

Due to both ethical and technical restrictions, the events of early embryonic development in many mammals remains elusive. During these early developmental stages, gastrulation occurs – an important event induced by trophoblast-epiblast signalling and sets up the embryo body plan. At approximately the same developmental stage, the amnion will form. The amnion plays an import role later in development by surrounding and protecting the foetus, however relatively little is known about its early role in embryonic development. The amnion forms in one of two ways, depending on species. In some mammals, the amnion will form by a cavitation mechanism and in others it will form by a folding mechanism. Interestingly, in species where the amnion forms by folding, the trophoblast overlying the epiblast disappears. In cavitating species, the overlying trophoblast remains.

This correlation between trophoblast disappearance or persistence and the mechanism of amnion formation, is the basis for the hypothesis of central epiblast shielding. This hypothesis states that the central epiblast must be shielded from gastrulation-inducing signals that originate from the trophoblast. This shielding can occur in one of two ways. Epiblast cavitation ensures that the central epiblast is shielded from the gastrulation-inducing signals of the trophoblast by distance, while removal of the overlying trophoblast also achieves central epiblast shielding but without the necessity of cavity formation. However, in the guinea pig embryo, the trophoblast and the epiblast are already separated before the cavity forms. How is gastrulation induced without an epiblast-trophoblast boundary? Furthermore, why does the amniotic cavity still form when the central epiblast likely does not need to be shielded from any trophoblast signals?

In this study, we proposed a new role for the early amnion. We predict that the amniotic ectoderm (i.e. the roof of the epiblast cavity) has replaced the role of the trophoblast in the guinea pig embryo and is responsible for inducing gastrulation. Following on from this hypothesis, we would further predict that the amniotic cavity still forms in the guinea pig embryo to shield the central epiblast from the gastrulation-inducing signals coming from the amniotic ectoderm. To determine if this is true, I examined signalling in the peri-gastrulation guinea pig embryo. I characterised the peri-gastrulation guinea pig embryo and found that the trophoblast is not required to induce gastrulation. This is compatible with the hypothesis that the amniotic ectoderm is responsible for inducing gastrulation in the guinea pig embryo and, by extension, that central epiblast shielding remains important in the guinea pig embryo.