Figure 5. TMEM14C is not required for mitochondrial iron homeostasis.

(A) Quantitation of cellular iron status by ⁵⁵Fe metabolic labeling shows that basal cellular iron import is not decreased in Tmem14c-deficient MEL cells. However, cellular iron content is decreased in Tmem14c-deficient erythroid cells during differentiation. (B) Deficiency in heme synthesis in Tmem14c-silenced cells is not due to a defect in mitochondrial iron content. Inductively coupled plasma analysis of mitochondrial iron shows that Tmem14c deficiency does not cause a defect in mitochondrial iron content either basally or during erythroid differentiation (left). This was confirmed by ⁵⁹Fe metabolic labeling and quantitation of mitochondrial iron from differentiating Tmem14c-silenced cells (right). (C) Normal activities for [2Fe-2S] cofactor–dependent mitochondrial aconitase, FECH, and cytosolic xanthine oxidase in Tmem14c-silenced cells exclude defects in [2Fe-2S] cluster assembly. *P < 0.05.