Dr. Bates’s research program is focused on genetic mouse models of kidney and lower urinary tract development, given that congenital kidney and bladder diseases are leading causes of pediatric chronic kidney disease. One major focus is on the role of fibroblast growth factor receptors (FGFRs) in kidney development. Using conditional knockout and receptor point mutation approaches, the lab has uncovered many different roles for FGFRs in different lineages within the kidney. Many of these mice have features that mimic structural kidney disease in children, including renal aplasia, hypoplasia, and progressive cystic disease. Recently the lab has shown that FGFRs are critical for maintenance of nephron progenitors, the stem cell–like cells that eventually form nephrons in the kidney. A second major focus is on the roles of FGFR2 in ureteric bud induction, ureter function, and bladder function. Mice with deletion of FGFR2 in the mesenchymal cells in these tissues develop high rates of vesicoureteral reflux (backflow of urine from the bladder to the kidney), ureter contractile defects, and bladder structural and functional defects, including poor compliance and decreased contractility. As the mice age, they develop hydronephrosis and progressive kidney disease and apparent myogenic failure in the bladder. The lab also has found that deletion of FGFRs in bladder urothelium leads to significant patterning defects. Given the diverse actions of FGFRs throughout the developing mouse kidney and lower urinary tract, the lab plans on examining whether children with structural kidney and/or bladder diseases have permutations in FGF ligands and/or FGFRs.