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. 2008 Feb 22;105(9):3374–3379. doi: 10.1073/pnas.0712145105

Fig. 1.

Fig. 1.

Sirt1 is necessary for autophagy. (A) Transient expression of wild-type (WT) Sirt1 but not a deacetylase-inactive (HY) point mutant of Sirt1 stimulates conversion of LC3-I to LC3-II in HCT116 cells. Quantification of the relative (rel.) levels of LC3-II/LC3-I is shown with the ratio of 1.0 being assigned to vector-transfected cells under fed conditions. (B and C) Distribution of GFP-LC3 in HCT116 cells under fed conditions when transfected along with either a control empty vector (B) or when cotransfected with wild-type Sirt1 (C). (D) The deacetylase-inactive mutant of Sirt1 acts in a dominant-negative fashion to inhibit starvation-induced conversion of LC3-I to LC3-II in HCT116 cells. (E) Quantification of GFP-LC3 punctae in wild-type (+/+) and Sirt1−/− MEFs under fed or starved conditions. (F) Level of autophagy under fed or starved conditions in Sirt1−/− MEFs transfected with GFP-LC3 along with an empty vector, wild-type Sirt1, or the described deacetylase-inactive mutant, Sirt1 (HY).