Extended Data Fig. 2: The catalytic function of ALDOA is required for proliferation.
a) Viability of Akt1myr;MycOE;Trp53–/– cells after AldoA depletion (shAldoA) or control (shRen) or after silencing and re-expression of wild type AldoA (shAldoA_WT), a mutant unable to bind to actin (shAldoA_R43A) or a catalytically inactive mutant (shAldoA_K146Q). Inducible silencing and re-expression were achieved by treating cells with doxycycline (1 µg/ml) for 96 h. Data are presented as mean values ± SD. Significance was calculated using a two-tailed student’s t-test with FDR correction (n = 4 biologically independent replicates). b) Lysates from the cells shown in a) were analysed for expression of AldoA by Western blotting. Vinculin is shown as loading control. c) Viability of NrasG12V;MycOE;Trp53–/– cells after AldoA depletion (shAldoA) or control (shRen) or after silencing and re-expression of wild type AldoA (shAldoA_WT) or a catalytically inactive mutant (shAldoA_D34S). Inducible silencing and re-expression were achieved by treating cells with doxycycline (1 µg/ml) for 96 h. Data are presented as mean values ± SD. Significance was calculated using a two-tailed student’s t-test with FDR correction (n = 3 biologically independent replicates). d) Viability of Akt1myr;MycOE;Cdkn2aARF-/- cells after AldoA depletion (shAldoA) or control (shRen) or after silencing and re-expression of wild type AldoA (shAldoA_WT) or a catalytically inactive mutant (shAldoA_D34S). Inducible silencing and re-expression were achieved by treating cells with doxycycline (1 µg/ml) for 96 h. Data are presented as mean values ± SD. Significance was calculated using a two-tailed student’s t-test with FDR correction (n = 3 biologically independent replicates).
