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

SOD mimetics EUK-8 and EUK-134 restore normal O₂^•− levels and rescue defective NSCs in Fip200^GFAP 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.