Fig. 8.

Sall1 and Mi2β genetically interact during embryonic kidney development. (A–D) E15.5 kidneys dissected from genetic crosses between Sall1^+/−, Mi2β^fl/+ and Six2-Cre^tg/+, Mi2β^fl/+. Renal hypoplasia was seen in Sall1^+/−/Mi2β^Δ/+ double heterozygotes (B) and even more prominently in Mi2β^Δ/Δ (C) and Sall1^+/−, Mi2β^Δ/Δ (D) compared to Sall1^+/− (A) and wild type (data not shown) mice. (E–L) Histological analysis of Sall1/Mi2β compound mutants. Thickness of the nephrogenic zone (bracket) was reduced in Sall1^+/−/ Mi2β^Δ/+ double heterozygous kidneys (F, J); The loss of nephrogenic zone in Mi2β^Δ/Δ kidneys was more severe (G, K). In Sall1^+/−, Mi2β^Δ/Δ mutant kidneys the nephrogenic zone was not detected at this stage and there were rare differentiated structures (H, L). Sall1^+/− kidneys had a normal nephrogenic zone with many epithelial nephron precursor structures (E, I).