CDX2 is essential for cell proliferation and polarity in porcine blastocysts

Abstract

The role of CDX2 in trophectoderm (TE) cells has been extensively studied, yet the results are contradictory and species specific. Here, CDX2 expression and function were explored in early porcine embryos. Notably, siRNA-mediated gene knockdown and lentivirus-mediated TE-specific gene regulation demonstrated that CDX2 is essential for the maintenance of blastocyst integrity by regulating the BMP4-mediated blastocyst niche and classical protein kinase C (PKC)-mediated TE polarity in mammalian embryos. Mechanistically, CDX2-depleted porcine embryos stalled at the blastocyst stage and exhibited apoptosis and inactive cell proliferation possibly resulting from BMP4 downregulation. Moreover, TE cells in CDX2-depleted blastocysts displayed defective F-actin apical organization associated with downregulation of PKCα. Collectively, these results provide further insight into the functional diversity of CDX2 in early mammalian embryos.