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Inositol Depletion Restores Vesicle Transport in Yeast Phospholipid Flippase Mutants

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Title: Inositol Depletion Restores Vesicle Transport in Yeast Phospholipid Flippase Mutants
Authors: Yamagami, Kanako Browse this author
Yamamoto, Takaharu Browse this author →KAKEN DB
Sakai, Shota Browse this author
Mioka, Tetsuo Browse this author
Sano, Takamitsu Browse this author →KAKEN DB
Igarashi, Yasuyuki Browse this author →KAKEN DB
Tanaka, Kazuma Browse this author →KAKEN DB
Issue Date: 17-Mar-2015
Publisher: Public Library Science
Journal Title: Plos one
Volume: 10
Issue: 3
Start Page: e0120108
Publisher DOI: 10.1371/journal.pone.0120108
Abstract: In eukaryotic cells, type 4 P-type ATPases function as phospholipid flippases, which translocate phospholipids from the exoplasmic leaflet to the cytoplasmic leaflet of the lipid bilayer. Flippases function in the formation of transport vesicles, but the mechanism remains unknown. Here, we isolate an arrestin-related trafficking adaptor, ART5, as a multicopy suppressor of the growth and endocytic recycling defects of flippase mutants in budding yeast. Consistent with a previous report that Art5p downregulates the inositol transporter Itr1p by endocytosis, we found that flippase mutations were also suppressed by the disruption of ITR1, as well as by depletion of inositol from the culture medium. Interestingly, inositol depletion suppressed the defects in all five flippase mutants. Inositol depletion also partially restored the formation of secretory vesicles in a flippase mutant. Inositol depletion caused changes in lipid composition, including a decrease in phosphatidylinositol and an increase in phosphatidylserine. A reduction in phosphatidylinositol levels caused by partially depleting the phosphatidylinositol synthase Pis1p also suppressed a flippase mutation. These results suggest that inositol depletion changes the lipid composition of the endosomal/TGN membranes, which results in vesicle formation from these membranes in the absence of flippases.
Rights: http://creativecommons.org/licenses/by/4.0/
Type: article
URI: http://hdl.handle.net/2115/58975
Appears in Collections:遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 田中 一馬

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