Claudin-10a deficiency shifts proximal tubular Cl- permeability to cation selectivity via claudin-2 translocation

The tight junction (TJ) proteins claudin-2 and -10a form paracellular cation and anion channels, respectively, and have both been reported to be expressed in the proximal tubule (PT). However, the physiological role of claudin-10a in the kidney is yet obscure. Mice deficient in claudin-10a were generated and successful knockout was confirmed by Southern Blot, Western Blot and immunofluorescence staining. The functionality of isolated PTs was investigated electrophysiologically. Compensatory regulation was studied by pharmacological intervention, RNA-Seq analysis, Western Blot and immunofluorescence staining. 7 samples from proximal tubule (4 WT, 3 Cldn10a KO), 8 samples from distal convoluted tubule (4 WT, 4 Cldn10a KO)