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. Author manuscript; available in PMC: 2018 Mar 1.
Published in final edited form as: Nat Cell Biol. 2017 Jul 31;19(9):1061–1070. doi: 10.1038/ncb3586

Figure 2. cGAS facilitates oxidative stress-induced senescence.

Figure 2

(a, b, c, d) WT MEFs, cGAS KO MEFs or STING KO MEFs were cultured under hyperoxic conditions (40% O2) for 7 days and subsequently stained for SA-β-Gal activity (a), examined for percentages of EdU+ cells by immunofluorescence (b) or assessed for expression of Cdkn2a by RT-qPCR (c) or p16Ink4a by immunoblotting (d). (e) WI-38 cells were exposed to 40% O2 treatment for 9 days. On day 7 cells were transfected with a non-targeting control siRNA (si Control) or with siRNAs against cGAS (si cGAS #1, si cGAS #2). Expression of cGAS was assessed by immunoblotting on day 9. (f, g, h) WI-38 cells were treated as in (e). On day 9 SA-β-Gal activity was assessed by FACS (f) and expression of CDKN2A was examined by RT-qPCR (g) or p16Ink4a was assessed by immunoblotting (h). Numbers in (f) indicate percentages of SA-β-Gal positive cells. Mean and s.d. of n=5 independent experiments (a) or n=3 biological replicates (b, c, g) or one representative experiment out of 3 (f) or 2 (d, e, h) independent experiments are shown. P values were calculated by one-way (a) and two-way (b, c, g) ANOVA (* P < 0.05, ** P < 0.01, ns = not significant). Source data are available in Supplementary Table 1. Unprocessed original blots are shown in Supplementary Fig. 7.