Johnson D R, Knoll L J, Levin D E, Gordon J I
Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, Missouri 63110.
J Cell Biol. 1994 Nov;127(3):751-62. doi: 10.1083/jcb.127.3.751.
Saccharomyces cerevisiae has been used as a model for studying the regulation of protein N-myristoylation. MyristoylCoA:protein N-myristoyl-transferase (Nmt1p), is essential for vegetative growth and uses myristoylCoA as its substrate. MyristoylCoA is produced by the fatty acid synthetase (Fas) complex and by cellular acylCoA synthetases. We have recently isolated three unlinked Fatty Acid Activation (FAA) genes encoding long chain acylCoA synthetases and have now recovered a fourth by genetic complementation. When Fas is active and NMT1 cells are grown on media containing a fermentable carbon source, none of the FAA genes is required for vegetative growth. When Fas is inactivated by a specific inhibitor (cerulenin), NMT1 cells are not viable unless the media is supplemented with long chain fatty acids. Supplementation of cellular myristoylCoA pools through activation of imported myristate (C14:0) is predominantly a function of Faa1p, although Faa4p contributes to this process. Cells with nmt181p need larger pools of myristoylCoA because of the mutant enzyme's reduced affinity for this substrate. Faa1p and Faa4p are required for maintaining the viability of nmt1-181 strains even when Fas is active. Overexpression of Faa2p can rescue nmt1-181 cells due to activation of an endogenous pool of C14:0. This pool appears to be derived in part from membrane phospholipids since overexpression of Plb1p, a nonessential lysophospholipase/phospholipase B, suppresses the temperature-sensitive growth arrest and C14:0 auxotrophy produced by nmt1-181. None of the four known FAAs is exclusively responsible for targeting imported fatty acids to peroxisomal beta-oxidation pathways. Introduction of a peroxisomal assembly mutation, pas1 delta, into isogenic NMT1 and nmt1-181 strains with wild type FAA alleles revealed that when Fas is inhibited, peroxisomes contribute to myristoylCoA pools used by Nmt1p. When Fas is active, a fraction of cellular myristoylCoA is targeted to peroxisomes. A NMT1 strain with deletions of all four FAAs is still viable at 30 degrees C on media containing myristate, palmitate, or oleate as the sole carbon source--indicating that S. cerevisiae contains at least one other FAA which directs fatty acids to beta-oxidation pathways.
酿酒酵母已被用作研究蛋白质N-肉豆蔻酰化调控的模型。肉豆蔻酰辅酶A:蛋白质N-肉豆蔻酰转移酶(Nmt1p)对于营养生长至关重要,并以肉豆蔻酰辅酶A作为其底物。肉豆蔻酰辅酶A由脂肪酸合成酶(Fas)复合物和细胞酰基辅酶A合成酶产生。我们最近分离出了三个不连锁的脂肪酸激活(FAA)基因,它们编码长链酰基辅酶A合成酶,现在通过基因互补又获得了第四个。当Fas活跃且NMT1细胞在含有可发酵碳源的培养基上生长时,营养生长不需要任何一个FAA基因。当Fas被一种特异性抑制剂(浅蓝菌素)失活时,除非培养基补充长链脂肪酸,否则NMT1细胞无法存活。通过激活导入的肉豆蔻酸(C14:0)来补充细胞肉豆蔻酰辅酶A库主要是Faa1p的功能,尽管Faa4p也参与了这个过程。由于突变酶对该底物的亲和力降低,具有nmt181p的细胞需要更大的肉豆蔻酰辅酶A库。即使Fas活跃,Faa1p和Faa4p对于维持nmt1-181菌株的活力也是必需的。Faa2p的过表达可以挽救nmt1-181细胞,这是由于激活了内源性的C14:0库。这个库似乎部分来源于膜磷脂,因为非必需的溶血磷脂酶/磷脂酶B Plb1p的过表达抑制了nmt1-181产生的温度敏感型生长停滞和C14:0营养缺陷型。四个已知的FAA中没有一个专门负责将导入的脂肪酸靶向过氧化物酶体β-氧化途径。将过氧化物酶体组装突变pas1 delta引入具有野生型FAA等位基因的同基因NMT1和nmt1-181菌株中,结果表明当Fas被抑制时,过氧化物酶体对Nmt1p使用的肉豆蔻酰辅酶A库有贡献。当Fas活跃时,一部分细胞肉豆蔻酰辅酶A被靶向到过氧化物酶体。一个缺失所有四个FAA的NMT1菌株在含有肉豆蔻酸、棕榈酸或油酸作为唯一碳源的培养基上于30℃仍可存活,这表明酿酒酵母至少还含有另一种将脂肪酸导向β-氧化途径的FAA。