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. Author manuscript; available in PMC: 2015 Sep 1.
Published in final edited form as: Traffic. 2014 Jul 12;15(9):933–945. doi: 10.1111/tra.12188

Figure 6. Regulation of PE export from mitochondria to the ER.

Figure 6

Newly synthesized PS is imported from the ER to mitochondria, converted to PE and then exported back to the ER. The export of PE seems to be regulated by Ups1 and Ups2. X indicates a putative PE transfer protein. Broken lines indicate movements of phospholipids. Bold and thin broken lines depict accelerated and decelerated phospholipid transports, respectively. Our pulse chase experiments have suggested that (B) loss of Ups2 accelerates PE export from mitochondria to the ER, leading to decreased levels of PE and increased levels of PC (71). (C) In contrast, loss of Ups1 appears to slow the PE export. The loss of Ups1 also leads to decreased steady state levels of Psd1 probably due to low membrane potential (ΔΨ) across the IM under the fermentable condition (70, 71). (D) The decreased ΔΨ in the absence of Ups1 is restored under the non-fermentable condition, which restores ΔΨ (61).