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The primary cilium is required during early embryo patterning, epithelial tubulogenesis, and growth factor-dependent signal transduction. The requirement for primary cilia during renal epithelial-mesenchymal tissue interactions that give rise to nephrons is undefined. Here, we used  Cre- mediated recombination to generate mice with  Kif3a  deficiency targeted to the ureteric and/or metanephric mesenchyme cell lineages in the embryonic kidney. Gradual loss of primary cilia in either lineage leads to a phenotype of reduced nephron number. Remarkably, in addition to cyst formation, loss of primary cilia in the ureteric epithelial cell leads to decreased expression of  Wnt11  and  Ret  and reduced ureteric branching. Constitutive expression of GLI3 repressor ( Gli3 Δ699/+  ) rescues these abnormalities. In embryonic metanephric mesenchyme cells,  Kif3a  deficiency limits survival of nephrogenic progenitor cells and expression of genes required for nephron formation. Together, our data demonstrate that  Kif3a  controls nephron number via distinct cell lineage-specific mechanisms.

Kif3a Controls Murine Nephron Number Via GLI3 Repressor, Cell Survival, and Gene Expression in a Lineage-Specific Manner