Figure 2 |. Nephron formation is defective in Six2-Qpc^−/− mutant mice.

(a) Shown are representative immunofluorescence images of formalin-fixed, paraffin-embedded kidney sections from Cre⁻ littermate control and Six2-Qpc^−/− mice at age postnatal day (P) 0, stained for megalin, thiazide-sensitive sodium chloride cotransporter (NCC), and Wilms tumor 1 protein (WT1). Ureteric buds are outlined by dashed white lines. The white arrows identify positive staining. Bar = 50 −m. (b) Quantification of megalin-NCC–expressing nephron segments and glomeruli in control and Six2-Qpc^−/− mice. Shown is positively stained area or number of glomeruli (Glom) per mm². Glomerular and nephron segment–specific gene expression in total kidney homogenates from Six2-Qpc^−/− mutants at age P0. Gene expression was compared with Cre⁻ littermate controls and expressed as fold change (n = 5 each). Data represent mean ± SEM; Student’s t test, 2-tailed, *P < 0.05, **P < 0.01, and ***P < 0.001. Aqp1, aquaporin 1; Aqp2, aquaporin 2; CD, collecting duct; DT, distal tubule; glo, glomerular; mTAL, medullary thick ascending loop of Henle; NaPi2a, sodium-phosphate cotransporter 2A; Nkcc2, sodium-potassium-chloride cotransporter 2; PT, proximal tubule; Rel, relative; Scnn1a, epithelial sodium channel 1 alpha subunit; Trpv5, transient receptor potential cation channel subfamily V member 5; Umod, uromodulin. To optimize viewing of this image, please see the online version of this article at www.kidney-international.org.