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. 2016 Mar 28;212(7):879. doi: 10.1083/jcb.20150702303082016c

Correction: Elevated p62/SQSTM1 determines the fate of autophagy-deficient neural stem cells by increasing superoxide

Chenran Wang, Song Chen, Syn Yeo, Gizem Karsli-Uzunbas, Eileen White, Noboru Mizushima, Herbert W Virgin, Jun-Lin Guan
PMCID: PMC4810301  PMID: 27002165

Vol. 212 No. 5, February 29, 2016. Pages 545–560.

After publication, the authors discovered an error in Fig. 8 J. In the published version, arrowheads were inadvertently left out of the image. The authors apologize for this error. The corrected image is included below.

Figure 8.

Figure 8.

SOD mimetics EUK-8 and EUK-134 restore normal O2 levels and rescue defective NSCs in Fip200GFAP cKO mice. (A–I) Ctrl and Fip200 GFAP cKO mice at P28 were treated with vehicle, EUK-8, or EUK-134. (A) DHE and DAPI fluorescence in SVZ. Arrows indicate SVZ cells. Dotted lines indicate the boundaries of the SVZ (n = 4 mice each). (B) Mean ± SEM of SVZ cellularity per section (n = 3 mice each). (C and D) Mean ± SEM of GFAP+Nestin+ (C) and GFAP+SOX2+ (D) cells per section (n = 4 mice each). (E and F) Mean ± SEM of the percentage of GFAP+Nestin+Ki67+ to total Ki67+ cells (E) or total GFAP+Nestin+ cells (F) in SVZ (n = 4 mice each). (G–I) Mean ± SEM of TUNEL+ (G) or DCX+ (H) cells per SVZ section and NeuN+ cells in the OB per square millimeter (I) of mice (n = 4 mice each). E, ependymal layer; LV, lateral ventricle; ST, striatum. Bars, 50 µm. *, P < 0.05; **, P < 0.01; ***, P < 0.001. (J) A working model of differential p62 aggregate formation and O2 •− accumulation by deletion of Fip200, but not Atg5, Atg16L1, or Atg7, leading to defective neural stem cell maintenance and differentiation.

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