| First Author | Heckt T | Year | 2016 |
| Journal | Biochem Biophys Res Commun | Volume | 469 |
| Issue | 4 | Pages | 1069-74 |
| PubMed ID | 26731031 | Mgi Jnum | J:233156 |
| Mgi Id | MGI:5780899 | Doi | 10.1016/j.bbrc.2015.12.104 |
| Citation | Heckt T, et al. (2016) No obvious phenotypic abnormalities in mice lacking the Pate4 gene. Biochem Biophys Res Commun 469(4):1069-74 |
| abstractText | We have previously reported that the hormone calcitonin (CT) negatively regulates bone formation by inhibiting the release of sphingosine-1-phosphate from bone-resorbing osteoclasts. In the context of this study we additionally observed that CT repressed the expression of Pate4, encoding the secreted protein caltrin/Svs7, in osteoclasts from wildtype mice. To assess a possible function of Pate4 in bone remodeling, we utilized commercially available embryonic stem cells with a targeted Pate4 allele to generate Pate4-deficient mice. These were born at the expected Mendelian ratio and did not display obvious abnormalities until the age of 6 months. A bone-specific histomorphometric analysis further revealed that bone remodeling is unaffected in male and female Pate4-deficient mice. Since a subsequently performed multi-tissue expression analysis confirmed that Pate4 is primarily expressed in prostate and seminal vesicles, we additionally analyzed the respective tissues of Pate4-deficient mice, but failed to detect histological abnormalities. Most importantly, as assessed by mating with female wildtype mice, we did not observe reduced fertility associated with Pate4-deficiency. Taken together, our study was the first to generate and analyze a mouse model lacking Pate4, a gene with strong expression in prostate and seminal vesicles, yet without major function for fertility. |
