Objectives: The Odd-skipped related 1 (Osr1) and Odd-skipped related 2 (Osr2) encode zinc finger transcription factors required for accurate segment formation in the embryonic development. Mouse Osr2 has been shown to share a 65% homology with Osr1 and 100% homology in zinc finger domain. Osr2 is expressed in the mandible/maxilla, limb, testis, and lung. The function of Osr2 in the hard tissue is not fully understood, though Osr2 is expressed during limb and mandible/maxilla development. Methods: To analyze the function of Osr2 in bone development, transgenic mice were generated using dominant negative Osr2 driven by a 5kb mouse Osr2 gene promoter (Osr2deltaN Tg). The genotype was confirmed by PCR of tail genome using transgene-specific primers. Results: The growth was significantly retarded in Osr2deltaN Tg compared with wild type mice. At 3 weeks after birth, soft X-ray analysis of transgenic mice revealed markedly increased radiolucency compared with the wild type. Judged by skeletons of newborn mice stained with alcian blue and alizarin red, those intensities of skull and skeletal elements of Osr2deltaN Tg were apparently reduced. Morphologically, calvaria of Osr2deltaN Tg composed of markedly thinner parietal bones and less number of osteoblastic cells on parietal bone surfaces, which indicates delayed intramembranous ossification. RT-PCR analysis revealed that expressions of osteoblast marker genes were significantly reduced or scarcely detected in primary osteoblastic cells of Osr2deltaN Tg, those included alkaline phosphatase, osteocalcin, Runx2, and osterix. Conclusions: These findings indicate that Osr2 play an important role during the process of parietal periosteal bone formation.

Back to the Mineralized Tissue Program
Back to the IADR General Session & Exhibition (June 28 – July 1, 2006)

Top Level Search