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Pluripotent epiblast (EPI) cells, present in the inner cell mass (ICM) of the mouse blastocyst, are progenitors of both embryonic stem (ES) cells and the fetus. Discovering how pluripotency genes regulate cell fate decisions in the blastocyst provides a valuable way to understand how pluripotency is normally established. EPI cells are specified by two consecutive cell fate decisions. The first decision segregates ICM from trophectoderm (TE), an extraembryonic cell type. The second decision subdivides ICM into EPI and primitive endoderm (PE), another extraembryonic cell type. Here, we investigate the roles and regulation of the pluripotency gene  Sox2  during blastocyst formation. First, we investigate the regulation of  Sox2  patterning and show that SOX2 is restricted to ICM progenitors prior to blastocyst formation by members of the HIPPO pathway, independent of CDX2, the TE transcription factor that restricts  Oct4  and  Nanog  to the ICM. Second, we investigate the requirement for  Sox2  in cell fate specification during blastocyst formation. We show that neither maternal (M) nor zygotic (Z)  Sox2  is required for blastocyst formation, nor for initial expression of the pluripotency genes  Oct4  or  Nanog  in the ICM. Rather, Z  Sox2  initially promotes development of the primitive endoderm (PE) non cell-autonomously via FGF4, and then later maintains expression of pluripotency genes in the ICM. The significance of these observations is that 1) ICM and TE genes are spatially patterned in parallel prior to blastocyst formation and 2) both the roles and regulation of  Sox2  in the blastocyst are unique compared to other pluripotency factors such as  Oct4  or  Nanog .

HIPPO Pathway Members Restrict SOX2 to the Inner Cell Mass Where It Promotes ICM Fates in the Mouse Blastocyst