Fig. 2

Sirt6 is required for OSK-induced MEF reprogramming. a Alkaline phosphatase staining showed reduced MEF reprogramming efficiency in Sirt6-null MEFs. b Oct4-GFP-positive clones were shown in both wild-type and Sirt6-null OG2 MEFs after fully reprogramming. c Quantification of Oct4-GFP-positive clones showed reduced MEF reprogramming efficiency in Sirt6-null OG2 MEFs. Sirt6-null OG2 MEFs were reprogrammed by introducing OSK, and the number of fully reprogrammed GFP-positive clones was counted. Data represented mean ± SD from three independent assays (*, p ≤ 0.05). d Quantification of AP-positive clones showed reduced tail-tip fibroblast (TTF) reprogramming efficiency in Sirt6-null TTFs. Sirt6-null TTFs were reprogrammed by introducing OSK. Data represented mean ± SD from three independent assays (***, p ≤ 0.001). e Oct4-GFP-positive clone counting showed a ~ 2-fold increase in Sirt6-null OG2 MEF reprogramming efficiency upon overexpression of Sirt6. The reprogramming efficiencies were detected using OSK reprogramming factors. The data were shown as mean values ± SD from three independent experiments. (*, p ≤ 0.05). f Downregulation of Sirt6 decreased the generation of iPSCs. Alkaline phosphatase staining of pre-iPSC clones in wild-type OG2 MEFs transduced with three factors OSK in two siRNA of Sirt6 and in non-target group. g The number of GFP-positive clones was counted in wild-type OG2 MEFs transduced with three factors OSK in two siRNA of Sirt6 and in the non-target group. All data were shown as mean values ± SD from three independent experiments. (**, p ≤ 0.01; ***, p ≤ 0.001)