Erratum: Selected missense mutations impair frataxin processing in Friedreich ataxia.

[This corrects the article DOI: 10.1002/acn3.433.].

In Clark et al. (2017)1 figure legends for figure 5 and 6 were incorrectly published on pages 581–582.

Legends for figure 5 and 6 were switched and should have read as:

Figure 5. Impaired FXN processing from FXN42–210 to FXN81–210 occurs in fibroblasts from FRDA patients with FXNG130V. FXN levels were quantified by western blot using whole cell extracts from control (CTRL), FRDA, and G130V patient fibroblasts. CTRL = 5 fibroblast lines (n = 13), G130V = 3 lines (n = 17), and Typical = 7 lines (n = 8). (A) FXN42–210 (18 kD), and FXN81–210 (13 kD) levels from control (CTRL), G130V, and typical FRDA were detected from whole cell extracts by western blot using an anti‐FXN antibody. Detection of GAPDH serves as a loading control. FXN levels are quantified and expressed as a ratio of FXN42–210 to FXN81–210. (*) = P < 0.05. (B). Confocal microscopy images of patient fibroblasts (CTRL, FRDA, and G130V) that were fixed and stained using primary anti‐FXN and primary antimitofusin antibodies. Secondary antibodies included Alexa Fluor 568 (FXN) and Alexa Fluor 488 (mitofusin). DAPI was also used as a nuclear stain.

Figure 6. Increasing FXNG130V and FXNI154F FXN1–210 levels does not increase FXN81–210 levels. Following transfection of HEK 293 cells with mutant FXN constructs, cells were treated with 10 lmol/L MG132 proteasome inhibitor for 5 h followed by cell lysis. Exogenous FXN1–210 (23 kD), FXN42–210 (19 kD), and FXN81–210 (15 kD) levels, before and after treatment, were detected by western blot using a primary anti‐HA antibody.

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