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. 2016 Nov 23;26(2):354–366. doi: 10.1093/hmg/ddw392

Figure 4.

Figure 4.

Expression of BAC transgene carrying Flcn H255Y mutant allele does not rescue kidney-targeted Flcn knockout mouse phenotype. (A) Histology of Flcn-deficient kidney with Flcn H255Y mutant expression (Flcn f/d/H255Y, CDH16-Cre) at 3 weeks of age compared to Flcn-deficient kidney (Flcn f/d, CDH16-Cre) and control kidney (Flcnf/+, CDH16-Cre). Multi-cystic kidneys are shown with hyperplastic kidney cells protruding into the cystic lumen in both Flcn f/d/H255Y, CDH16-Cre mice and Flcn f/d, CDH16-Cre mice. (B) Kidney to body weight ratio of kidney-targeted Flcn knockout mice with Flcn H255Y mutant expression (Flcn f/d/H255Y, CDH16-Cre) at 3 weeks of age compared to kidney-targeted Flcn knockout mice (Flcn f/d, CDH16-Cre) and control mice (Flcnf/+, CDH16-Cre). No significant difference was seen between Flcn f/d/H255Y, CDH16-Cre and Flcn f/d, CDH16-Cre mice. (C) Kaplan-Meier survival plot of kidney-targeted Flcn knockout mice with Flcn H255Y mutant expression compared to kidney-targeted Flcn knockout and control mice; n= 8 mice for each genotype. No significant difference was seen between Flcn f/d/H255Y, CDH16-Cre and Flcn f/d, CDH16-Cre mice. (D) Western blot analysis of mTORC1 downstream effectors in Flcn-deficient kidneys with Flcn H255Y mutant expression, Flcn-deficient kidneys and control kidneys. N.S., no significance.