Figure 6
From: Mechanism of cystogenesis by Cd79a-driven, conditional mTOR activation in developing mouse nephrons
Heterozygous loss of Raptor suppresses cystogenesis in Cd79a-Tsc1 knockout (KO) kidneys. (a) Representative images of kidney sections from control, Cd79a-Cre;Tsc1ff., and Cd79a-Cre;Raptorf/+;Tsc1ff. (Cd79a-Raptor Hetero;Tsc1 KO) mice at 4 and 6 weeks of age. (b) Comparison of cystic index at 4 and 6 weeks of age. Heterozygous loss of Raptor effectively suppresses cyst formation in Cd79a-Tsc1 KO kidneys. (c) Western blot analysis. Whole kidney lysates from each group were blotted with p-S6 and p-Akt antibodies. p-S6 expression was significantly reduced in Cd79a-Raptor Hetero;Tsc1 KO mice compared with Cd79a-Tsc1 KO mice. p-Akt expression did not differ among the three groups. The original gels was shown in Supplementary Fig. S13. (d) Quantification of cilia length (at 4 and 6 weeks) and mTOR signals. p-S6 and p-Akt signals were quantified from the immunoblot shown in (c). Concomitant heterozygous loss of Raptor reduced cilia length and p-S6 abundance in Cd79a-Tsc1 KO kidneys to a level comparable to control kidneys, suggesting that the cilia length defect is mediated by the mTORC1 complex. Values represent mean ± SEM and statistical significance was determined by one-way ANOVA. **P < 0.01, ***P < 0.001 and ****P < 0.0001.
