title: No obvious phenotypic abnormalities in mice lacking the Pate4 gene.
abstract: 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.
authors.affiliation: Department of Osteology and Biomechanics, University Medical Center Hamburg Eppendorf, Hamburg 20246, Germany.
authors.forename: Timo
authors.initials: T
authors.lastname: Heckt
authors.affiliation: Department of Osteology and Biomechanics, University Medical Center Hamburg Eppendorf, Hamburg 20246, Germany.
authors.forename: Johannes
authors.initials: J
authors.lastname: Keller
authors.affiliation: Central Animal Facility, University Medical Center Hamburg Eppendorf, Hamburg 20246, Germany.
authors.forename: Roswitha
authors.initials: R
authors.lastname: Reusch
authors.affiliation: Insitute of Neuropathology, University Medical Center Hamburg Eppendorf, Hamburg 20246, Germany.
authors.forename: Kristin
authors.initials: K
authors.lastname: Hartmann
authors.affiliation: Insitute of Neuropathology, University Medical Center Hamburg Eppendorf, Hamburg 20246, Germany.
authors.forename: Susanne
authors.initials: S
authors.lastname: Krasemann
authors.affiliation: Center of Molecular Neurobiology, University of Hamburg, Hamburg 20251, Germany.
authors.forename: Irm
authors.initials: I
authors.lastname: Hermans-Borgmeyer
authors.affiliation: Department of Osteology and Biomechanics, University Medical Center Hamburg Eppendorf, Hamburg 20246, Germany.
authors.forename: Michael
authors.initials: M
authors.lastname: Amling
authors.affiliation: Department of Osteology and Biomechanics, University Medical Center Hamburg Eppendorf, Hamburg 20246, Germany. Electronic address: schinke@uke.uni-hamburg.de.
authors.forename: Thorsten
authors.initials: T
authors.lastname: Schinke
mesh_terms: D000015:Abnormalities, Multiple / Q000235:genetics*; D000818:Animals; D001862:Bone Resorption / Q000235:genetics*; D002352:Carrier Proteins / Q000235:genetics*; D020022:Genetic Predisposition to Disease / Q000235:genetics; D051379:Mice / Q000235:genetics*; D018345:Mice, Knockout; D010641:Phenotype; D029607:Seminal Vesicle Secretory Proteins / Q000235:genetics*
chemical_list: D002352:Carrier Proteins; C430719:Pate4 protein, mouse; D029607:Seminal Vesicle Secretory Proteins
keywords: Bone remodeling; Calcitonin; Pate4; Seminal vescicle; Svs7