Figure 4.

Loss of one copy of Spry1 rescues NPC death and proliferation defects caused by loss of Fgf9 and Fgf20. (A–F) Six2 staining of E11.5 Fgf9, Fgf20, and Spry1 compound mutant kidneys. (G) Quantifying the number of nephron progenitors of Fgf9, Fgf20, and Spry1 compound mutant kidneys, showing that deleting one copy of Spry1 restored loss of nephron progenitors. (H–M) Pax2 and EdU staining of E11.5 Fgf9, Fgf20, and Spry1 compound mutant kidneys. (N) Proliferation index of Fgf9, Fgf20, and Spry1 compound mutant kidneys, showing that deleting one copy of Spry1 restored nephron progenitor proliferation defects. (O–T) Pax2 and terminal deoxynucleotidyl transferase–mediated digoxigenin-deoxyuridine nick-end labeling (Tunel) staining of E11.5 Fgf9, Fgf20, and Spry1 compound mutant kidneys. (U) Cell death index of Fgf9, Fgf20, and Spry1 compound mutant kidneys, showing that deleting one copy of Spry1 rescued NPC death. Data are shown with mean±SD. *P<0.01. Scale bar, 100 µm.