| First Author | Li Q | Year | 2005 |
| Journal | J Biol Chem | Volume | 280 |
| Issue | 4 | Pages | 2831-9 |
| PubMed ID | 15546883 | Mgi Jnum | J:95901 |
| Mgi Id | MGI:3527984 | Doi | 10.1074/jbc.M405680200 |
| Citation | Li Q, et al. (2005) A targeted mutation of Nkd1 impairs mouse spermatogenesis. J Biol Chem 280(4):2831-9 |
| abstractText | Nkd1 is an antagonist of the canonical Wnt/beta-catenin signaling pathway. The EF-hand motif of Nkd1 is required for its inhibitory function. Early studies suggested that Nkd1 might play important roles in mouse embryonic development and tumorigenesis. We constructed Nkd1(-/-) mice whose Nkd1 protein lacked the EF-hand and was unable to inhibit Wnt/beta-catenin signaling. The homozygotes were viable and grew normally, but their fertility in males was reduced. In wild-type adult testes, Nkd1 mRNA was expressed more abundantly in the elongating spermatids than in the round spermatids. Lack of EF-hand caused reductions in the testis weight and sperm count by 30 and 60%, respectively. During testis development, Nkd1 mRNA expression started at the 25th day after birth, coincident with the onset of Wnt1 expression. Nuclear localization of beta-catenin increased in the elongating spermatids, suggesting that the mutant Nkd1 failed to inhibit the Wnt/beta-catenin pathway. These results suggest that deletion of the EF-hand from Nkd1 reduces the number of the elongating spermatids at haploid stage. In contrast, the mutant Nkd1 did not affect intestinal polyposis in Apc(Delta716) mice. |
