Figure 5.
Figure 5. Loss of ACBD5 or VAPB reduces PO membrane expansion in Mff-deficient fibroblasts. PO morphology in Mff-deficient fibroblasts (control; A) after reintroduction of Mff (B) or silencing of Pex11β (C), ACBD5 (D), or VAPB (E). Fixed cells were labeled with anti-Pex14 antibodies. (F) Quantification of PO morphology in controls and silenced cells (n = 2,500, from three independent experiments). Data are presented as mean ± SEM. ***, P < 0.001; ns, not significant. (G) Immunoblots of cell lysates. Loading controls used were catalase (Cat), GAPDH, and thioredoxin (Thiored). (H–M) Localization of endogenous ACBD5 in Mff-deficient fibroblasts. Fixed cells labeled with anti-ACBD5 and anti-catalase antibodies. Arrowheads denote ACBD5 concentrated at globular POs that give rise to tubular membranes. Bars, 10 µm.

Loss of ACBD5 or VAPB reduces PO membrane expansion in Mff-deficient fibroblasts. PO morphology in Mff-deficient fibroblasts (control; A) after reintroduction of Mff (B) or silencing of Pex11β (C), ACBD5 (D), or VAPB (E). Fixed cells were labeled with anti-Pex14 antibodies. (F) Quantification of PO morphology in controls and silenced cells (n = 2,500, from three independent experiments). Data are presented as mean ± SEM. ***, P < 0.001; ns, not significant. (G) Immunoblots of cell lysates. Loading controls used were catalase (Cat), GAPDH, and thioredoxin (Thiored). (H–M) Localization of endogenous ACBD5 in Mff-deficient fibroblasts. Fixed cells labeled with anti-ACBD5 and anti-catalase antibodies. Arrowheads denote ACBD5 concentrated at globular POs that give rise to tubular membranes. Bars, 10 µm.

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