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. Author manuscript; available in PMC: 2020 Jun 4.
Published in final edited form as: Cell Metab. 2019 Mar 28;29(6):1274–1290.e9. doi: 10.1016/j.cmet.2019.03.001

Fig. 3. P53 regulates sirtuins at the transcriptional and posttranscriptional level in telomere dysfunctional mice.

Fig. 3

(a) Luciferase assay with Sirt1-7 promoter sequences in pGL3 vector shows increased Sirt3, 4 & 5 luciferase activity in G4/p53 −/− compared to G4 /p53 +/+ MEFs (pGL3 vector and p21 promoter serve as background and positive controls); (b) Luciferase assays with Sirt1-7 3’UTR reveals increased luciferase activity in G4/p53 −/− MEFs compared to G4/p53 +/+ MEFs; (c) Polysome analyses in WT, p53 −/−, G4/p53 +/+, and G4/p53 −/− MEFs shows increased polysome occupancy of Sirt1, 2, 6, 7 transcripts in G4/p53 −/− MEFs (two independent experiments); (d) Western blot analysis of MEFs treated with proteasome inhibitor MG132 indicates that Sirt7 protein abundance is also regulated by proteasome-mediated degradation; (e) RT-qPCR analysis of WT MEFs transduced with PGC-1α - expressing adenovirus shows that PGC-1α overexpression in MEFs induces Sirt3, 4 & 5 mRNA levels; (f) Western blot analysis of MEFs overexpressing PGC-1α or GFP demonstrates that PGC-1α increases Sirt3, 4 & 5 protein abundance without affecting other sirtuins. Results are expressed as mean ± s.e.m. and are derived from three independent experiments in two MEF cell lines/genotype unless stated otherwise; t-test was used to determine statistical significance with p <0.05 considered as significant, as indicated by (*).