Igf1r signaling is indispensable for preimplantation development and is activated via a novel function of E-cadherin.

ABSTRACT: Insulin-like growth factor I receptor (Igf1r) signaling controls proliferation, differentiation, growth, and cell survival in many tissues; and its deregulated activity is involved in tumorigenesis. Although important during fetal growth and postnatal life, a function for the Igf pathway during preimplantation development has not been described. We show that abrogating Igf1r signaling with specific inhibitors blocks trophectoderm formation and compromises embryo survival during murine blastocyst formation. In normal embryos total Igf1r is present throughout the membrane, whereas the activated form is found exclusively at cell contact sites, colocalizing with E-cadherin. Using genetic domain switching, we show a requirement for E-cadherin to maintain proper activation of Igf1r. Embryos expr

SUBMITTER: Bedzhov I 

PROVIDER: S-EPMC3315466 | biostudies-literature | 2012

REPOSITORIES: biostudies-literature