From the Department of Food Science, Rutgers Center for Lipid Research, and New Jersey Institute for Food, Nutrition, and Health, Rutgers University, New Brunswick, New Jersey 08901 and.
J Biol Chem. 2013 Oct 4;288(40):29124-33. doi: 10.1074/jbc.M113.507392. Epub 2013 Aug 22.
In the yeast Saccharomyces cerevisiae, the DGK1-encoded diacylglycerol kinase catalyzes the CTP-dependent phosphorylation of diacylglycerol to form phosphatidate. This enzyme, in conjunction with PAH1-encoded phosphatidate phosphatase, controls the levels of phosphatidate and diacylglycerol for phospholipid synthesis, membrane growth, and lipid droplet formation. In this work, we showed that a functional level of diacylglycerol kinase is regulated by the Reb1p transcription factor. In the electrophoretic mobility shift assay, purified recombinant Reb1p was shown to specifically bind its consensus recognition sequence (CGGGTAA, -166 to -160) in the DGK1 promoter. Analysis of cells expressing the PDGK1-lacZ reporter gene showed that mutations (GT→TG) in the Reb1p-binding sequence caused an 8.6-fold reduction in β-galactosidase activity. The expression of DGK1(reb1), a DGK1 allele containing the Reb1p-binding site mutation, was greatly lower than that of the wild type allele, as indicated by analyses of DGK1 mRNA, Dgk1p, and diacylglycerol kinase activity. In the presence of cerulenin, an inhibitor of de novo fatty acid synthesis, the dgk1Δ mutant expressing DGK1(reb1) exhibited a significant defect in growth as well as in the synthesis of phospholipids from triacylglycerol mobilization. Unlike DGK1, the DGK1(reb1) expressed in the dgk1Δ pah1Δ mutant did not result in the nuclear/endoplasmic reticulum membrane expansion, which occurs in cells lacking phosphatidate phosphatase activity. Taken together, these results indicate that the Reb1p-mediated regulation of diacylglycerol kinase plays a major role in its in vivo functions in lipid metabolism.
在酵母酿酒酵母中,DGK1 编码的二酰基甘油激酶催化 CTP 依赖性磷酸化二酰基甘油形成磷酸酯。该酶与 PAH1 编码的磷酸酯酶一起控制磷酸酯和二酰基甘油的水平,以进行磷脂合成、膜生长和脂质滴形成。在这项工作中,我们表明二酰基甘油激酶的功能水平受到 Reb1p 转录因子的调节。在电泳迁移率变动分析中,纯化的重组 Reb1p 被证明特异性结合其在 DGK1 启动子中的共识识别序列(CGGGTAA,-166 至-160)。表达 PDGK1-lacZ 报告基因的细胞分析表明,Reb1p 结合序列中的突变(GT→TG)导致β-半乳糖苷酶活性降低 8.6 倍。含有 Reb1p 结合位点突变的 DGK1(reb1)的表达,如 DGK1 mRNA、Dgk1p 和二酰基甘油激酶活性分析所示,比野生型等位基因大大降低。在新脂肪酸合成抑制剂 Cerulenin 的存在下,表达 DGK1(reb1)的 dgk1Δ 突变体在生长以及从三酰基甘油动员合成磷脂方面表现出明显缺陷。与 DGK1 不同,在缺乏磷酸酯酶活性的细胞中,dgk1Δ pah1Δ 突变体中表达的 DGK1(reb1)不会导致核/内质网膜扩张。总之,这些结果表明 Reb1p 介导的二酰基甘油激酶的调节在其体内脂质代谢功能中起着主要作用。