PTH signaling is a target of several anabolic osteoporosis treatments. Gsα, a subunit of the heterotrimeric Gs protein, mediates PTH activity via a signaling pathway involving adenylate cyclase, cyclic AMP (cAMP), and protein kinase A (PKA). Previous studies have found a severe decrease in bone mineral density to be associated with deleting Gsα early in development. In this study, we investigate the effects of a post-natal Gsα deletion on osteogenic gene expression. Using Cre-Tet transgenic mice under a Tet-off expression system, doxycycline was administered from conception until weaning as a means of preventing a Gsα deletion from taking place prenatally. To analyze gene expression in wildtype and Gsα knockout mice, RNA was first extracted followed by reverse transcription into cDNA. The cDNA was then analyzed for levels of gene expression via qPCR. Significantly decreased expression of Gsα in the Gsα knockout mice was consistent with the identity of these mice being knockout mice. Although no significant changes in expression of OSX, Col 1, and BSP were observed between Gsα knockout and wild-type mice, significantly decreased expression of osteocalcin and osteopontin, genes positively regulated by PTH, were found in the Gsα knockout mice. Since Gsα mediates PTH signaling, we reasoned a post-natal deletion of Gsα leads to decreased PTH activity and based on our findings, a decreased expression of osteogenic genes positively regulated by PTH. Overall, this study demonstrates that Gsα indirectly affects expression of osteogenic genes transcriptionally regulated by PTH.