Recent models propose that the extra-embryonic ectoderm supports the growth of the embryo and is a source of signals for A-P axis establishment [29]. To address whether the developmental defects of Bptf mutants are caused by defective extra-embryonic ectoderm or by a lack of appropriate growth signals in the epiblast, we monitored the expression of the extra embryonic ectoderm (Bmp4, Erbb2, Fgfr2), trophectoderm (Mash2), angiogenesis (Vegf, Flk1) and a cell cycle regulator (JunB) markers [43]–[47]. We find Bmp4, Mash2, Erbb2, and Fgfr2 to be expressed normally in the mutant embryos at E6.5 and E7.5 (Figure S11A, Figure S11B). This suggests that the growth defects observed in Bptf embryos are not due to gross defects in the specification the extra-embryonic tissues. We also observe little to no expression of the angiogenesis markers Vegf and Flk1 in the extra-embryonic tissues at E7.5 (Figure S11B). However, expression of the cell cycle regulator JunB is increased in mutant embryonic ectoderm when compared to wild-type controls (Figure S11A). JunB is a member of the Ap-1 family of transcription factors which acts as a negative regulator
