Sevlever D, Schiemann D, Guidubaldi J, Medof M E, Rosenberry T L
Department of Pharmacology, Case Western Reserve University, Cleveland, OH 44106, U.S.A.
Biochem J. 1997 Feb 1;321 ( Pt 3)(Pt 3):837-44. doi: 10.1042/bj3210837.
Glucosaminyl(acyl)phosphatidylinositol [GlcN(acyl)PI], the third intermediate in the mammalian glycosylphosphatidylinositol (GPI) anchor pathway, is undetectable in most cells. This intermediate was previously shown to accumulate, however, in murine lymphoma mutant E and in yeast mutant dpm1, both of which lack dolicholphosphomannose synthase activity. Here we report that a mammalian HeLa S3 subline, denoted D, produces large amounts of GlcN(acyl)PI. The level of GlcN(acyl)PI in this subline is twice that in the murine lymphoma mutant E and 4 times that in the parental S3 line. This HeLa D subline differs from the previously reported mutants that accumulate GlcN(acyl)PI because no defects in the synthesis or utilization of dolicholphosphomannose were found. Kinetic analysis indicated that in this HeLa subline there is an increased rate of synthesis of GlcN(acyl)PI, whereas the rate of metabolism for this GPI is comparable to that in wild-type cells. Furthermore, HeLa D cells accumulate GlcN(acyl)PI without a block in the synthesis of the downstream mannosylated GPI anchor precursors and GPI-anchored proteins. These findings might be relevant for understanding the regulation of the GPI pathway.
N-乙酰葡糖胺(酰基)磷脂酰肌醇[GlcN(acyl)PI]是哺乳动物糖基磷脂酰肌醇(GPI)锚定途径中的第三个中间体,在大多数细胞中无法检测到。然而,先前已证明该中间体在小鼠淋巴瘤突变体E和酵母突变体dpm1中积累,这两种突变体均缺乏多萜醇磷酸甘露糖合酶活性。在此我们报告,一种名为D的哺乳动物HeLa S3亚系会产生大量的GlcN(acyl)PI。该亚系中GlcN(acyl)PI的水平是小鼠淋巴瘤突变体E中的两倍,是亲本S3系中的四倍。这个HeLa D亚系与先前报道的积累GlcN(acyl)PI的突变体不同,因为未发现多萜醇磷酸甘露糖的合成或利用存在缺陷。动力学分析表明,在这个HeLa亚系中,GlcN(acyl)PI的合成速率增加,而这种GPI的代谢速率与野生型细胞中的相当。此外,HeLa D细胞积累GlcN(acyl)PI时,下游甘露糖基化GPI锚定前体和GPI锚定蛋白的合成没有受阻。这些发现可能与理解GPI途径的调控有关。