Rosales Fritz V M, Maccioni H J
CIQUIBIC (UNC-CONICET), Departamento di Química Biológica, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Argentina.
J Neurochem. 1995 Oct;65(4):1859-64. doi: 10.1046/j.1471-4159.1995.65041859.x.
Ganglioside GT3 is the precursor of c-series gangliosides. It is synthesized by sialylation of GD3 and is expressed in nervous tissue of birds and mammals at early stages of development. In this study we examined the sub-Golgi location of GT3 synthesis and the mechanism of its transport from the site of synthesis to the plasma membrane in chicken embryo retina cells in culture. Neural retina cells from 10-day-old chick embryo were cultured with [3H]galactose in the absence (control cells) or in the presence of 1 micrograms/ml brefeldin A (BFA). At the end of the labeling period, the fraction of labeled gangliosides transported to the plasma membrane was determined. For this, cells were treated with C. perfringens neuraminidase in conditions to desialylate only those gangliosides that were transported to the plasma membrane and consequently accessible to the enzyme. After neuraminidase treatment of cells, gangliosides were isolated, purified, and the pattern of radioactivity analyzed by HPTLC-fluorography. It was found that BFA blocked the synthesis of complex gangliosides without affecting the synthesis of GM3, GD3, and GT3. Furthermore, in BFA-treated cells, GM3, GD3, and GT3 were protected from the action of added neuraminidase, indicating an intracellular localization and, hence, an inhibition of their transport to the plasma membrane. The results indicate that synthesis of the first intermediates of a-, b-, and c- series gangliosides occurs in a proximal Golgi compartment and that the proximal Golgi-synthesized gangliosides (GM3, GD3, and GT3) use a transport mechanism that is dependent on ADP ribosylation factor and coatomer proteins.
神经节苷脂GT3是c系列神经节苷脂的前体。它由GD3经唾液酸化合成,在鸟类和哺乳动物发育早期的神经组织中表达。在本研究中,我们检测了GT3合成在高尔基体下的位置以及其在培养的鸡胚视网膜细胞中从合成位点转运至质膜的机制。将10日龄鸡胚的神经视网膜细胞在无(对照细胞)或有1微克/毫升布雷菲德菌素A(BFA)存在的情况下用[3H]半乳糖培养。在标记期结束时,测定转运至质膜的标记神经节苷脂的比例。为此,在仅使那些转运至质膜并因此可被该酶作用的神经节苷脂去唾液酸化的条件下,用产气荚膜梭菌神经氨酸酶处理细胞。对细胞进行神经氨酸酶处理后,分离、纯化神经节苷脂,并通过高效薄层层析荧光成像分析放射性模式。发现BFA阻断了复合神经节苷脂的合成,而不影响GM3、GD3和GT3的合成。此外,在BFA处理的细胞中,GM3、GD3和GT3受到添加的神经氨酸酶作用的保护,表明其定位于细胞内,因此其转运至质膜受到抑制。结果表明,a、b和c系列神经节苷脂的首批中间体在高尔基体近端区室合成,且高尔基体近端合成的神经节苷脂(GM3、GD3和GT3)使用一种依赖于ADP核糖基化因子和外被体蛋白的转运机制。