Figure 1.

ATM is critical for oncogene-induced senescence. (A) SA-β-gal staining of human diploid fibroblasts IMR90 infected with control vector or ca-STAT5A. The percent of SA-β-gal-positive cells is indicated at the bottom of each panel. The percent of cells that incorporate BrdU is shown below the panels. (B) Indirect immunofluorescence showing p53 induction by ca-STAT5A in cells fixed 8 d after infection. (C) Quantitation of ATM protein levels in IMR90 infected with a control hairpin or the anti-ATM hairpin vector. (D) Indirect p53 immunofluorescence in IMR90 cells expressing the indicated vectors. The staining intensity is translated into a color code using Metamorph software. (E) Rescue of ca-STAT5A-induced senescence by shRNA against ATM measured by SA-β-gal staining. IMR90 cells bearing the empty vector LXSN or its derivatives expressing E6 or E7 were infected with an empty vector or its derivative expressing an shRNA against ATM together with STAT5A1*6. The percent and standard deviation of SA-β-gal-positive cells are indicated at the bottom right of each panel. Data represent three independent experiments done with cells collected 6 d post-selection. (F) Rescue of RasV12-induced senescence by shRNA against ATM measured by SA-β-gal staining. Fibroblasts bearing the empty vector LXSN or its derivative expressing E7 were infected with an empty vector or its derivative expressing an shRNA against ATM together with RasV12. The percent and standard deviation of SA-β-gal-positive cells are indicated at the bottom right of each panel. Data represent three independent measurements done with cells fixed 14 d post-selection.