Yamamoto Takaharu, Fujimura-Kamada Konomi, Shioji Eno, Suzuki Risa, Tanaka Kazuma
Graduate School of Life Science, Division of Molecular Interaction, Institute for Genetic Medicine, Hokkaido University, Sapporo 060-0815, Japan.
Graduate School of Medicine, Division of Molecular Interaction, Institute for Genetic Medicine, Hokkaido University, Sapporo 060-0815, Japan.
G3 (Bethesda). 2017 Jan 5;7(1):179-192. doi: 10.1534/g3.116.035238.
Type 4 P-type ATPases (P4-ATPases) function as phospholipid flippases, which translocate phospholipids from the exoplasmic leaflet to the cytoplasmic leaflet of the lipid bilayer, to generate and maintain asymmetric distribution of phospholipids at the plasma membrane and endosomal/Golgi membranes. The budding yeast Saccharomyces cerevisiae has four heteromeric flippases (Drs2p, Dnf1p, Dnf2p, and Dnf3p), associated with the Cdc50p family noncatalytic subunit, and one monomeric flippase, Neo1p They have been suggested to function in vesicle formation in membrane trafficking pathways, but details of their mechanisms remain to be clarified. Here, to search for novel factors that functionally interact with flippases, we screened transposon insertional mutants for strains that suppressed the cold-sensitive growth defect in the cdc50Δ mutant. We identified a mutation of YMR010W encoding a novel conserved membrane protein that belongs to the PQ-loop family including the cystine transporter cystinosin and the SWEET sugar transporters. We named this gene CFS1 (cdc fifty suppressor 1). GFP-tagged Cfs1p was partially colocalized with Drs2p and Neo1p to endosomal/late Golgi membranes. Interestingly, the cfs1Δ mutation suppressed growth defects in all flippase mutants. Accordingly, defects in membrane trafficking in the flippase mutants were also suppressed. These results suggest that Cfs1p and flippases function antagonistically in membrane trafficking pathways. A growth assay to assess sensitivity to duramycin, a phosphatidylethanolamine (PE)-binding peptide, suggested that the cfs1Δ mutation changed PE asymmetry in the plasma membrane. Cfs1p may thus be a novel regulator of phospholipid asymmetry.
4型P型ATP酶(P4-ATP酶)作为磷脂翻转酶发挥作用,它将磷脂从脂质双分子层的外质小叶转运至细胞质小叶,以在质膜和内体/高尔基体膜上产生并维持磷脂的不对称分布。出芽酵母酿酒酵母有四种异源翻转酶(Drs2p、Dnf1p、Dnf2p和Dnf3p),与Cdc50p家族非催化亚基相关,还有一种单体翻转酶Neo1p。它们被认为在膜运输途径的囊泡形成中起作用,但其机制细节仍有待阐明。在此,为了寻找与翻转酶功能相互作用的新因子,我们筛选了转座子插入突变体,以寻找能抑制cdc50Δ突变体中冷敏感生长缺陷的菌株。我们鉴定出YMR010W的一个突变,该基因编码一种新的保守膜蛋白,属于PQ环家族,包括胱氨酸转运体胱氨酸病蛋白和SWEET糖转运体。我们将这个基因命名为CFS1(cdc50抑制因子1)。绿色荧光蛋白标记的Cfs1p与Drs2p和Neo1p部分共定位于内体/晚期高尔基体膜。有趣的是,cfs1Δ突变抑制了所有翻转酶突变体的生长缺陷。因此,翻转酶突变体中膜运输的缺陷也得到了抑制。这些结果表明,Cfs1p和翻转酶在膜运输途径中起拮抗作用。一项评估对短杆菌肽(一种结合磷脂酰乙醇胺(PE)的肽)敏感性的生长试验表明,cfs1Δ突变改变了质膜中PE的不对称性。因此,Cfs1p可能是磷脂不对称性的一种新调节因子。