| dc.description.abstract | Beta-catenin (CTNNB1) is a key downstream effector of the WNT signaling pathway, a pathway involved in embryonic development and tumorigenesis. To further study the role of CTNNB1 in gut tumorigenesis, mice homozygous for a conditional stabilizing mutation of Ctnnb1(a floxed allele) were crossed with mice hemizygous for a Cre recombinase under a gut-specific promoter (Villin-Cre). However, contrary to expectations of Mendelian inheritance, no double heterozygous mice (Ctnnb1flox, Villin-Cre) were observed at birth, suggesting embryonic lethality. Since the WNT signaling pathway is involved in embryonic development, and previous studies have confirmed the expression of Villin in the visceral yolk, this study primarily focused on potential placental defects that may have caused the lethality. After assessment of the embryonic lethality which occurred between embryonic stage 11.5 and 13.5, a Rosa26reporter was crossed with Villin-Cre and the resulting embryos and placentae were stained to localize the location of beta galactosidase activity. We found that Villin-Cre is expressed in the yolk sac epithelium, indicating potential defects in the hematopoiesis and/or cellular function caused by the Ctnnb1 mutation. We are currently assessing gene expression in yolk sac epitheliums by RNAseq to provide insights into the molecular changes caused by ectopic WNT signaling due to stabilization of CTNNB1. | |
