the fate of notchdeficient nephrogenic progenitor cells during metanephric kidney development to determine which nephron segments require notch signals for development we conditionally deleted rbpj a transcription factor required for canonical notch signaling in nephrogenic progenitors nps of the metanephric mesenchyme the retinoic acid receptor2 rarb2 promoter efficiently directed crerecombinase cre activity to these progenitors conditional knockout of rbpj in mice rarb2crerbpjf caused severe renal hypoplasia as indicated by a 7095 reduction in nephron number and the development of tubular cysts to track the fate of nps following rarb2cre expression we labeled them with membraneassociated enhanced green fluorescent protein gfp in tomatogfprarb2cre control mice nps differentiated into epithelia of all nephron segments except into collecting ducts in tomatogfprarb2crerbpjf conditional knockout mice nps developed into podocytes or distal tubular epithelia indicating that canonical notch signals were not required for mesenchymaltoepithelial transition or for the specification of these nephron segments conversely the few proximal tubules and associated cysts that developed in these mice were derived from the 510 of nps that had failed to express cre and therefore had intact notch signaling thus our fate mapping studies establish that the profound effect of notch signaling on nephrogenesis is due to the specification of proximal but not distal tubules or podocytes