Background: While urothelial signals, including sonic hedgehog (Shh), drive bladder mesenchyme differentiation, it is unclear which pathways within the mesenchyme are critical for its development. Studies have shown fibroblast growth factor receptor 2 (Fgfr2) is necessary for kidney and ureter mesenchymal development. Objective: Out objective was to determine the role of Fgfr2 in bladder mesenchyme. Methods: We used Tbx18cre mice to delete Fgfr2 in bladder mesenchyme (Fgfr2BM-/-). We performed three dimensional (3D) reconstructions, real time PCR (qPCR), in situ hybridization, immunolabeling, ELISAs, immunoblotting, void stain on paper (VSOP), ex vivo bladder sheet assays, and in vivo decerebrated cystometry. Results: Compared to controls, embryonic day (E) 16.5 Fgfr2BM-/- bladders have thin muscle layers with reduced alpha smooth muscle actin (αSMA) levels and thickened lamina propria with increased collagen expression that intrudes into muscle. From P1 to P30, Fgfr2BM-/- bladders demonstrate progressive muscle loss and increased collagen expression. Postnatal Fgfr2BM-/- bladder sheets exhibit decreased contractility and increased passive stretch tension vs. controls. In vivo cystometry revealed high baseline and threshold pressures and shortened intercontractile intervals in Fgfr2BM-/- bladders vs. controls. Mechanistically, while Shh expression appears normal, mRNA and protein readouts of hedgehog activity are increased in E16.5 Fgfr2BM-/- bladders vs. controls. Moreover, E16.5 Fgfr2BM-/- bladders exhibit higher levels of Cdo and Boc, hedgehog co-receptors that enhance sensitivity to Shh, vs. controls Conclusion: Fgfr2 is critical for bladder mesenchyme patterning by modulating hedgehog signaling.