Abstract
During blastocyst formation, inner cell mass (ICM) cells differentiate into either epiblast (Epi) or Primitive Endoderm (PrE) cells, labeled by Nanog and Gata6, respectively, and organized in a salt and pepper pattern. Previous work showed that in absence of Nanog all ICM cells adopt a PrE identity [1] . Moreover, the activation or the blockade of the Fgf/RTK pathway biases cell fate specification toward either PrE or Epi, respectively. We have also showed recently that in absence of Gata6 all ICM cells adopt an Epi identity. Moreover, the analysis of Gata6+/- embryos reveals a dosage sensitive phenotype, with less PrE specified cells [2] . These results and previous findings enabled the development of a mathematical model for the dynamics of the regulatory network controlling ICM differentiation into Epi or PrE cells (collaboration with the group of A. Goldbeter/G. Dupont, ULB Brussels) [2] . We will show here how our recent results integrate into the different hypotheses for the aetiology of Epi and PrE specification.
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