| First Author | Rivas B | Year | 2014 |
| Journal | Genesis | Volume | 52 |
| Issue | 4 | Pages | 328-32 |
| PubMed ID | 24443144 | Mgi Jnum | J:213360 |
| Mgi Id | MGI:5584231 | Doi | 10.1002/dvg.22742 |
| Citation | Rivas B, et al. (2014) Normal fertility in male mice with deletion of beta-catenin gene in germ cells. Genesis 52(4):328-32 |
| abstractText | As a dual function protein, beta-catenin affects both cell adhesion and mediates canonical Wnt/beta-catenin cell signaling. beta-Catenin is prominently expressed in somatic Sertoli cells in the testis and postmeiotic germ cells, suggesting an additional role in spermatogenesis. It was reported previously that Cre/loxP-mediated conditional inactivation of the beta-catenin gene (Ctnnb1) in male gonads using a protamine promoter-driven Cre transgene (Prm-cre) resulted in partial infertility, reduced sperm count, and abnormal spermatogenesis. In this report, we demonstrated that the conditional deletion of Ctnnb1 using a germ cell specific Cre transgene (Stra8-icre) had no effect on male fertility. We have shown that the Stra8-icre transgene was highly efficient in generating deletion in early pre-meiotic and post-meiotic cells. No differences in anatomical or histological presentation were found in the mutant testis, the production of viable sperm was similar, and no abnormalities in DNA sperm content were detected. We concluded that beta-catenin is fully dispensable in germ cells for spermatogenesis. The conflicting results from the earlier study may have been due to off-target expression of Prm-cre in testicular somatic cells. In future studies, the analysis of conditional mutants using several Cre-transgenes should be encouraged to reduce potential errors. |
