19The pluripotent epiblast gives rise to all tissues and organs in an adult body. Its differentiation starts 20 at gastrulation when the epiblast generates mesoderm and endoderm germ layers through a process 21 called epithelial-mesenchymal transition (EMT). Although gastrulation EMT coincides with loss of 22 epiblast pluripotency, pluripotent cells in development and in vitro can adopt either mesenchymal or 23 epithelial morphology. The relationship between epiblast's cellular morphology and its pluripotency is 24 not well understood. In this work, using chicken epiblast and mammalian pluripotency stem cell (PSC) 25 models, we show that PSCs undergo a mesenchymal-epithelial transition (MET) prior to EMT-26 associated pluripotency loss. Epiblast MET and its subsequent EMT are two distinct processes. The 27former, a partial MET, is associated with reversible initiation of pluripotency exit; whereas the latter, 28 a full EMT, is associated with complete and irreversible pluripotency loss. We provide evidence that 29integrin-mediated cell-matrix interaction is a key player in pluripotency exit regulation. We propose 30 that epiblast partial MET is an evolutionarily conserved process among all amniotic vertebrates and its 31 developmental function is to mediate planar symmetry-breaking within an epithelialized epiblast, 32 taking place after epiblast MET but before gastrulation EMT. 33 34 epiblast EMT and its pluripotency loss, we carried out a transcriptomic analysis of pre-and peri-97 gastrulation stage chicken embryos (HH1-HH3; 0.5h