期刊
DEVELOPMENTAL BIOLOGY
卷 288, 期 1, 页码 276-283出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ydbio.2005.09.045
关键词
uterus; myometrium; mullerian duct; mesenchyme; beta-catenin; adipogenesis; myogenesis
资金
- NICHD NIH HHS [F32HD43539, R01HD32112, U54 HD28138] Funding Source: Medline
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 Writ 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The uteri of adult conditional beta-catenin mutants are grossly deficient in smooth muscle of the myometrium, which has been replaced by adipose, a phenotype resembling human lipoleiomyoma.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. (C) 2005 Elsevier Inc. All rights reserved.
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