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. 2020 Aug 4;31(11):2559–2572. doi: 10.1681/ASN.2020040401

Figure 1.

Figure 1.

Loss of one copy of Spry1 rescues renal phenotypes caused by loss of Fgf9 and Fgf20. (A–F) Morphology of urogenital system in E18.5 Fgf9, Fgf20, and Spry1 compound mutants. (E) Renal agenesis caused by loss of Fgf9 and Fgf20 was restored by (F) deleting one copy of Spry1. * in (E) indicates loss of kidneys. (G–K) Hematoxylin and eosin staining of E18.5 kidneys of Fgf9, Fgf20, and Spry1 compound mutants. (I) Renal cysts of Fgf9-/+;Fgf20−/− animals disappeared after (J) deleting one copy of Spry1. (L–P) Sections of E18.5 kidneys stained with cytokeratin-8 (Cyt8) and Six2 in E18.5 kidneys of Fgf9, Fgf20, and Spry1 compound mutants. (N) Loss of NPCs caused by deletion of Fgf9 and Fgf20 were restored by (O and P) deleting one copy of Spry1. (L′–P′) High power image of nephrogenic zone. (Q) Percentage of kidney phenotypes and (R) relative kidney size of Fgf9, Fgf20, and Spry1 compound mutants. *P<0.01. Scale bar, 100 µm. K, kidney; B, bladder.