In this work, we aimed to determine the role of activin A during crucial events of mouse embryogenesis and distinguish the function of the protein of zygotic origin and the one secreted by the maternal reproductive tract. To this end, we recorded the progression of development and phenotype of Inhba knockout embryos and compared them with the heterozygotes and wild-type embryos using time-lapse imaging and detection of lineage-specific markers. We revealed that the zygotic activin A deficiency does not impair the course and rate of development of embryos to the blastocyst stage. Inhba knockout embryos form functional epiblast, as evidenced by their ability to give rise to embryonic stem cells. Our study is the first to show that derivation, maintenance in culture, and pluripotency of embryo-derived embryonic stem cells are exogenous and endogenous activin A independent. However, the implantation competence of activin A–deficient embryos may be compromised as indicated in the outgrowth assay.

Summary Sentence

The knockout of zygotic activin A affects neither the development of embryos to the blastocyst stage nor the derivation and maintenance of embryonic stem cells; however, it may impair the ability of embryos to implantation.

Graphical Abstract