and decreased phosphorylated histone H3 staining. A histological analysis of mutant embryos at E6.5 and E7.5 revealed that they develop a VE but do not form a primitive streak or differentiate mesoderm. To investigate the causes of the defect in gastrulation, we monitored the expression of key markers prior to and during gastrulation in the embryo. As anticipated we failed to observe expression of primitive streak markers T, Foxa2, Gsc, Fgf8 or the posterior localization of Nodal and Cripto expression. Defects in the expression of primitive streak markers and the delocalized expression of Nodal and Cripto are likely due to the absence of the DVE/AVE. Defects in the DVE/AVE were confirmed by observing significantly reduced expression of the markers Cer1, Hex1, Lefty1 and Hesx1 in E5.5 and E6.5 embryos. Defects in Gata6 expression at E5.5 suggest that the defects in DVE specification are accompanied by general defects in VE specification. From these studies we conclude that a critical function for Bptf during mammalian development is directly or indirectly to specify the VE and DVE after implantation.
