Abstract
Formation of a eutherian mammal requires concurrent establishment of embryonic and extraembryonic lineages. The functions of the trophectoderm and primitive endoderm are to enable implantation in the maternal uterus, axis specification and delivery of nutrients. The pluripotent epiblast represents the founding cell population of the embryo proper, which is protected from ectopic and premature differentiation until it is required to respond to inductive cues to form the fetus. While positional information plays a major role in specifying the trophoblast lineage, segregation of primitive endoderm from epiblast depends upon gradual acquisition of transcriptional identity, directed but not initiated by fibroblast growth factor (FGF) signalling. Following early cleavage divisions and formation of the blastocyst, cells of the inner cell mass lose totipotency. Developing epiblast cells transiently attain the state of naive pluripotency and competence to self-renew in vitro as embryonic stem cells and in vivo by means of diapause. This property is lost after implantation as the epiblast epithelializes and becomes primed in preparation for gastrulation and subsequent organogenesis.
Highlights
Mammalian preimplantation development combines establishment of a small population of founder cells for the fetus with early differentiation of extraembryonic tissues required to facilitate implantation, patterning and nutrition
Experiments in which isolated blastomeres from 4- and 8-cell stages were aggregated with host blastomeres from another embryo have shown that they are able to differentiate into both trophectoderm and inner cell mass (ICM) and yield viable pups [11]
In corroboration of this observation, the capacity for isolated epiblast cells to generate naive pluripotent cell lines in feeder-free 2i/leukaemia inhibitory factor (LIF) culture conditions is rapidly lost in the early postimplantation embryo [86], an event which functionally marks the exit from naive pluripotency in vivo
Summary
Mammalian preimplantation development combines establishment of a small population of founder cells for the fetus with early differentiation of extraembryonic tissues required to facilitate implantation, patterning and nutrition. The transcriptional and translational machinery becomes activated to institute self-sufficient cell populations from the maternally dominated zygote. The embryonic lineage must be protected from premature differentiation to remain susceptible to subsequent positional and temporal patterning in order to orchestrate formation of all the tissues in the body. This property is known as naive pluripotency [1]. We review the current knowledge of how this intriguing state of ‘naive’ pluripotency is acquired in vivo
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