The mammalian ureter is a tube connecting the kidney with the urinary bladder and it moves urine through its lumen by peristalsis. Moreover, ureter malformations cause human ill health. Despite these facts, the mechanisms of ureter development and differentiation have been little studied. Human ureter malformations have been reported to display transforming growth factor Î² (TGFÎ²) upregulation. I hypothesised that TGFÎ² has functional roles in normal and abnormal ureter morphogenesis. Tgfb1, Tgfb2, and Tgfb3 transcripts coding for TGFÎ² ligands, and Tgfbr1 and Tgfbr2 coding for TGFÎ² receptors, were detected by quantitative polymerase chain reaction in embryonic mouse ureters. As assessed by in situ hybridisation and immunohistochemistry, these receptors were detected in embryonic urothelia. Embryonic day 15 mouse ureters contain immature smooth muscle and urothelial layers and I used serum-free organ culture to model ureter growth, differentiation and acquisition of peristaltic function. Exogenous TGFÎ²1 inhibited growth of the ureter tube and generated cocoon-like dysmorphogenesis. RNA sequencing suggested that altered levels of certain fibroblast growth factors (FGFs) followed exposure to TGFÎ²1. In culture, exogenous FGF10 but not FGF18 abrogated certain dysmorphic effects mediated by TGFÎ²1. To assess whether an endogenous TGFÎ² axis functions in developing ureters, explants were exposed to TGFÎ² receptor chemical blockade; ureter growth was enhanced, and aberrant bud-like structures arose from the urothelial tube. The muscle layer was attenuated around these buds, and peristalsis was compromised. As for the mouse studies, immunostaining of normal embryonic human ureters detected TGFÎ²RI and TGFÎ²RII in urothelia. My observations reveal unsuspected regulatory roles for endogenous TGFÎ² in embryonic ureters, fine-tuning morphogenesis and functional differentiation. My results also support the hypothesis that the TGFÎ² upregulation reported in ureter malformations impacts on pathobiology. Next, taking advantage of the same ex vivo culture model, I also studied genetic models of urinary tract disease using mice with biallelic mutations of leucine rich repeats and immunoglobulin like domains (LRIG2) or heparanase (HPSE2). The equivalent human genes are mutated in urofacial syndrome, where defects in bladder innervation lead to severe voiding dysfunction and high bladder pressures. I showed that embryonic ureters from Lrig2 or Hpse2 mutant mice grew and underwent peristalsis as normal, and I concluded that the distended ureters that feature in this human disease are likely to be secondary to bladder dysfunction, rather than being intrinsic ureter defects. In conclusion, my thesis studies have illuminated the biology underlying normal and abnormal ureter morphogenesis.