| First Author | Arango NA | Year | 2005 |
| Journal | Dev Biol | Volume | 288 |
| Issue | 1 | Pages | 276-83 |
| PubMed ID | 16256976 | Mgi Jnum | J:103530 |
| Mgi Id | MGI:3610264 | Doi | 10.1016/j.ydbio.2005.09.045 |
| Citation | Arango NA, et al. (2005) Conditional deletion of beta-catenin in the mesenchyme of the developing mouse uterus results in a switch to adipogenesis in the myometrium. Dev Biol 288(1):276-83 |
| abstractText | Precise cell fate decisions during differentiation of uterine tissues from the embryonic Mullerian duct are critical for normal fertility. Wnt-7a, a member of the Wnt family of secreted signaling molecules that can signal through a canonical beta-catenin pathway, is necessary for the correct differentiation of both anterior/posterior and radial axes of the uterus. In order to investigate the role of beta-catenin directly in mouse uterine development, we have generated mice that are deficient in beta-catenin expression in the embryonic Mullerian duct. We have found that conditional deletion of beta-catenin in the Mullerian duct mesenchyme before postnatal differentiation of the uterine layers results in a phenotype that is distinct from the phenotype observed by deletion of Wnt-7a. Shortly after birth, the uteri of the conditional mutants appear smaller and less organized. The uteri of adult conditional beta-catenin mutants are grossly deficient in smooth muscle of the myometrium, which has been replaced by adipose, a phenotype resembling human lipoleiomyoma. We also show that the adipocytes in the uteri of mice conditionally deleted for beta-catenin are derived from Mullerian inhibiting substance type II receptor-expressing cells suggesting that they share a common origin with the uterine smooth muscle cells. These results describe the first molecular evidence linking disruption of beta-catenin expression in mesenchymal cells with a switch from myogenesis to adipogenesis in vivo. |
