Fig. 4: Loss of NTN1 causes DNA damage within LepR + MSCs.

a–c RNA-Seq analysis of LepR+ MSCs derived from young (5-6 month-old) LepR-NTN1 mice. a Heatmap depicting hierarchical clustering of differentially expressed genes. b GSEA demonstrating activation of DDR pathways in LepR+ cells of LepR-NTN1 mice. c GSEA Enrichment plots demonstrating activation of ADIPOGENESIS and DNA REPAIR pathways in LepR+ cells of LepR-NTN1 mice. d–f RNA-Seq analysis of LepR+ MSCs derived from CDH5-NTN1 mice. d Heatmap depicting hierarchical clustering of differentially expressed genes. e GSEA demonstrating activation of DDR pathways in LepR+ cells of CDH5-NTN1 mice. f GSEA Enrichment plots demonstrating activation of ADIPOGENESIS and DNA REPAIR pathways in LepR+ cells of CDH5-NTN1 mice. g Cell-cycle analysis of LepR+ MSCs derived from LepR-NTN1 mice and CDH5-NTN1 mice (N = 5 mice/group). h Representative IF images of single-cell gel electrophoresis (alkaline comet assays) performed on BM LepR+ MSCs. Alkaline comet analysis demonstrating an increase in average tail-moment and % Tail DNA in MSCs derived from both LepR-NTN1 mice i, and CDH5-NTN1 mice j, as compared to their littermate controls (N = 3 mice/group). Note that deletion of NTN1 within either MSCs or BMECs results in increased DNA damage within MSCs. Data is presented as the mean ± standard error of the mean (SEM). Statistical significance determined using two-tailed unpaired t-test. *P < 0.05; **P < 0.01; ***P < 0.001. ns denotes statistically not significant.