Fig. 2. Tubule-specific deletion of TMEM16a reduces cyst progression in an ADPKD mouse model.

a–d Western blotting from whole kidney lysates detecting tubule-specific deletion of Pkd1 (450 kDa) (^#P = 0.03) and increase in TMEM16A expression (glycosylated 130 kDa and non-glycosylated forms³⁴) (^#P = 0.003) (10 weeks after induction at postnatal days 20–22 using tamoxifen. Mice co-deleted for Pkd1 and Tmem16a (Pkd1^−/−/T16a^−/−) showed reduced Pkd1 expression (^#P = 0.022) and TMEM16A expression (^§P = 0.0004) (n = 3 animals each). e, f Tubule-specific knockout of Pkd1 (Pkd1^−/−) induced polycystic kidney disease (^#P < 0.0001, n = 11 animals), which was largely reduced in mice with an additional knockout of Tmem16a (Pkd1^−/−/T16a^−/−) (^§P = 0.0001, n = 11 animals). Non-induced Pkd1^fl;fl mice served as control (Pkd1^+/+) (n = 8 animals). Corresponding cystic indices (defined as cortical cyst area normalized to whole cortex area). Mean and error bars indicating ±SEM. ^#Unpaired two-sided t test comparing Pkd1^+/+ with Pkd1^−/−, ^§unpaired two-sided t test comparing Pkd1^−/− with Pkd1^−/−/T16a^−/−. Source data are provided as a Source Data file.