The porcine calcitonin receptor promoter directs expression of a linked reporter gene in a tissue and developmental specific manner in transgenic mice

We have investigated the transcriptional regulation of the porcine calciton in (CT) receptor (pCTR) promoter in transgenic mice. A construct containing 2.1 kb pCTR 5' flanking region, fused to a P-galactosidase (lacZ) gene, wa s employed for the production of transgenic mice. At 11.5 days of developme nt lacZ expression was observed in the embryonic brain and spinal cord. By 15.5 days post fertilization, lacZ expression was detected in the developin g mammary gland, external ear, cartilage primordium of the humerus, and ant erior naris (nostril). RT-PCR on RNA from these fetal tissues showed endoge nous mouse CTR (mCTR) expression. In neonatal and adult transgenics, lacZ e xpression was silenced, except in brain, spinal cord, and testis (adults on ly). Endogenous mCTR gene expression and pCTR promoter activity were corepr essed in the same tissues from adult mice. No pCTR promoter activity was de tected in the kidney or bone of transgenic animals. This suggests that addi tional DMA sequences may be required for pCTR promoter activity in these ti ssues. From these results, we conclude that the pCTR promoter is active onl y in tissues expressing endogenous mCTR. Many of the these tissues represen t previously unknown sites of CTR gene expression. Finally, the development al regulation of pCTR/mCTR in tissues such as breast and cartilage primordi um suggests that CTRs may play a role in the morphogenesis of these tissues .