ELO2 and ELO3, homologues of the Saccharomyces cerevisiae ELO1 gene, function in fatty acid elongation and are required for sphingolipid formation
ELO2 and ELO3, homologues of the Saccharomyces cerevisiae ELO1 gene, function in fatty acid elongation and are required for sphingolipid formation
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ELO2 和 ELO3 是酿酒酵母 ELO1 基因的同源物，它们在脂肪酸伸长过程中发挥作用，并且是鞘脂形成所必需的
DOI：
10.1074/jbc.272.28.17376
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发表时间：
1997-07-11
影响因子：
4.8
通讯作者：
Martin, CE
中科院分区：
文献类型：
--
作者：
Oh, CS;Toke, DA;Martin, CE
从酿酒酵母基因组数据库中鉴定出 ELO2 和 ELO3 是 ELO1 的同源物，ELO1 是一种参与脂肪酸 14:0 至 16:0 延伸的基因，这些基因中的突变先前已被证明可产生涉及许多膜功能的多效性效应，ELO2 和 ELO3 的同时破坏也已被证明可产生合成致死性，表明它们具有相关和/或重叠的功能，气相色谱法气相色谱/质谱分析表明，ELO2 和 ELO3 的 mull 突变在极长链脂肪酸的形成中产生缺陷。对无效突变体的分析表明，这些基因编码膜结合脂肪酸延伸系统的成分，该系统产生 26 碳极长链脂肪酸，这些脂肪酸是神经酰胺和鞘脂的前体。Elo2p 似乎参与了高达 24 个碳的脂肪酸的延伸，它似乎对链长小于 22 个碳的底物。 Elo3p 显然具有更广泛的底物特异性，并且对于将 24 碳酸转化为碳物种至关重要。任一基因的破坏都会降低细胞鞘脂水平并导致长链碱基植物鞘氨醇的积累。 ELO3 中的无效突变导致标记前体积累到肌醇磷酸神经酰胺中，而在更复杂的甘露糖化鞘脂中几乎没有标记，而 ELO2 的破坏导致所有鞘脂水平降低。
ELO2 and ELO3 were identified from the Saccharomyces cerevisiae genome data base as homologues of ELO1, a gene involved in the elongation of the fatty acid 14:0 to 16:0, Mutations in these genes have previously been shown to produce pleiotropic effects involving a number of membrane functions, The simultaneous disruption of ELO2 and ELO3 has also been shown to produce synthetic lethality, indicating that they have related and/or overlapping functions, Gas chromatography and gas chromatography/mass spectroscopy analyses reveal that mull mutations of ELO2 and ELO3 produce defects in the formation of very long chain fatty acids, Analysis of the null mutants indicates that these genes encode components of the membrane-bound fatty acid elongation systems that produce the 26-carbon very long chain fatty acids that are precursors for ceramide and sphingolipids, Elo2p appears to be involved in the elongation of fatty acids up to 24 carbons, it appears to have the highest affinity for substrates with chain lengths less than 22 carbons. Elo3p apparently has a broader substrate specificity and is essential for the conversion of 24-carbon acids to as carbon species. Disruption of either gene reduces cellular sphingolipid levels and results in the accumulation of the long chain base, phytosphingosine. Null mutations In ELO3 result in accumulation of labeled precursors into inositol phosphoceramide, with little labeling in the more complex mannosylated sphingolipids, whereas disruption of ELO2 results in reduced levels of all sphingolipids.