INAUGURAL ARTICLE, CELL BIOLOGY Correction for “Inaugural Article: Apoptosis is triggered when prosurvival Bcl-2 proteins cannot restrain Bax,” by Jamie I. Fletcher, Sarina Meusburger, Christine J. Hawkins, David T. Riglar, Erinna F. Lee, W. Douglas Fairlie, David C. S. Huang, and Jerry M. Adams, which appeared in issue 47, November 25, 2008, of Proc Natl Acad Sci USA (105: 18081–18087; first published November 3, 2008; 10.1073/pnas.0808691105).
The authors wish to add the following to the legend for Fig. 5B: “The vector and wt Bax control plots are identical to those shown in Fig. 2B because both the Bax D68R and Bax S184L mutants were run simultaneously with these controls in the same experiments.” This omission does not affect the conclusions of the article. The figure and its corrected legend appear below.
Fig. 5.
Enhanced killing when Bax D68R is forced onto membranes. (A) MEF may possess sufficient endogenous Bcl-xL (blue) to counter the small fraction of membrane-bound Bax D68R (orange) (Fig. 2A). This capacity might be overwhelmed if the predominantly cytosolic Bax D68R is driven onto membranes. (B) Bax S184L is fully functional. The viability of reconstituted bax−/−bak−/− MEF (described in Fig. 2A) after etoposide treatment (0–10 μM) for 24 h was assessed by propidium iodide exclusion using flow cytometry. The vector and wt Bax control plots are identical to those shown in Fig. 2B because both the Bax D68R and Bax S184L mutants were run simultaneously with these controls in the same experiments. (C) Combining the deregulated D68R mutation with S184L enhances Bax-mediated apoptosis. Colony formation was assessed for parental bax−/−bak−/− MEF, or these MEF stably overexpressing Bcl-xL, after infection with retroviruses expressing WT Bax or mutant (D68R, S184L, or D68R/S184L) forms of Bax. Data represent means ± 1 SEM of 3 or more independent experiments. Results were compared using two-tailed unpaired Student's t tests. ns, P > 0.05.