Fig. 4
Dissecting the role of CTD acetylation in binding. a Scheme of the treatments and p53 mutants. Expression levels of (HaloTag)-p53 upon the different treatments are shown. b Cumulative distribution of displacements (top) and complement cumulative distribution function of the single-molecule residence times (bottom) for control MCF-7/6/Hp53 cells, and cells transfected with a short-hairpin inhibiting the methyltransferase Set8 (3 replicates, n cells = 22, 23 for CTRL and Set8 Sh1, respectively). c Distribution of displacements (top) and complement cumulative distribution function of the single-molecule residence times (bottom) for HaloTag-p53-wt, HaloTag-p53-K382Q, or HaloTag-p53-6Q (acetylation mimicking mutants) transiently transfected in H1299 cells (insets, 3 replicates, n cells = 28, 24, and 18 for WT, K382Q, and 6Q, respectively). d Distribution of displacements for HaloTag-p53-wt (top, 2 replicates, n cells = 19 for no irradiation and 16 for 10 Gy IR) and p53-K382R (acetylation inhibiting mutant, bottom, 2 replicates, n cells = 16 for no irradiation and 15 for 10 Gy IR) transiently transfected in H1299 cells before and 2 h after irradiation (error bars: SD for bound fractions, 95% CI for average residence times)
