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Background  Beta-catenin is part of a protein complex associated with adherens junctions. When allowed to accumulate to sufficient levels in its dephosphorylated form, beta-catenin serves as a transcriptional co-activator associated with a number of signaling pathways, including steroid hormone signaling pathways.    Methods  To investigate the role of beta-catenin in progesterone (P 4 ) signaling and female reproductive physiology, conditional ablation of  Ctnnb1  from the endometrial mesenchymal ( i.e.  stromal and myometrial), but not epithelial, compartment was accomplished using the  Amhr2-Cre  mice. Experiments were conducted to assess the ability of mutant female mice to undergo pregnancy and pseudopregnancy by or through oil-induced decidualization. The ability of uteri from mutant female mice to respond to estrogen (E 2 ) and P 4  was also determined.    Results  Conditional deletion of  Ctnnb1  from the mesenchymal compartment of the uterus resulted in infertility stemming, in part, from complete failure of the uterus to decidualize. E 2 -stimulated epithelial cell mitosis and edematization were not altered in mutant uteri indicating that the mesenchyme is capable of responding to E 2 . However, exposure of ovariectomized mutant female mice to a combined E 2  and P 4  hormone regimen consistent with early pregnancy revealed that mesenchymal beta-catenin is essential for indirectly opposing E 2 -induced epithelial proliferation by P 4  and in some mice resulted in development of endometrial metaplasia. Lastly, beta-catenin is also required for the induced expression of genes that are known to play a fundamental role in decidualization such as  Ihh ,  Ptch1 ,  Gli1  and  Muc1Conclusions  Three salient points derive from these studies. First, the findings demonstrate a mechanistic linkage between the P 4  and beta-catenin signaling pathways. Second, they highlight an under appreciated role for the mesenchymal compartment in indirectly mediating P 4  signaling to the epithelium, a process that intimately involves mesenchymal beta-catenin. Third, the technical feasibility of deleting genes in the mesenchymal compartment of the uterus in an effort to understand decidualization and post-natal interactions with the overlying epithelium has been demonstrated. It is concluded that beta-catenin plays an integral role in selective P 4 -directed epithelial-mesenchymal communication in both the estrous cycling and gravid uterus.

Endometrial stromal beta-catenin is required for steroid-dependent mesenchymal-epithelial cross talk and decidualization