Ivanenkov Vasily V, Sévigny Jean, Kirley Terence L
Department of Pharmacology and Cell Biophysics, College of Medicine, University of Cincinnati, P.O. Box 670575, Cincinnati, Ohio 45267-0575, USA.
Biochemistry. 2008 Sep 2;47(35):9184-97. doi: 10.1021/bi800402q. Epub 2008 Aug 12.
Ecto-nucleoside triphosphate diphosphohydrolases, NTPDase1 (CD39) and NTPDase3, are integral plasma membrane proteins that hydrolyze extracellular nucleotides, thereby modulating the function of purinergic receptors. During processing in the secretory pathway, the active sites of ecto-nucleotidases are located in the lumen of vesicular compartments, thus raising the question whether the ecto-nucleotidases affect the ATP-dependent processes in these compartments, including protein folding in the endoplasmic reticulum (ER). It has been reported (J. Biol. Chem. (2001) 276, 41518-41525) that CD39 is not active until it reaches the plasma membrane, suggesting that terminal glycosylation in Golgi is critical for its activity. To investigate the subcellular location and the mechanism of ecto-nucleotidase activation, we expressed human NTPDase3 in COS-1 cells and blocked the secretory transport with monensin or brefeldin A, or by targeting to ER with a signal peptide. Cell surface biotinylation, sensitivity to glycosidases, and fluorescence microscopy analyses suggest that, in contrast to the previous report on CD39, NTPDase3 becomes catalytically active in the ER or in the ER-Golgi intermediate compartment, and that terminal glycosylation in Golgi is not essential for activity. Moreover, ER-targeted NTPDase3, but not wild-type NTPDase3 or ER-targeted inactive G221A mutant, significantly diminished the folding efficiency and the transport to the plasma membrane of coexpressed CD39 used as a reporter protein. These data suggest that ER-targeted NTPDase3 significantly depletes ATP in ER, whereas wild-type NTPDase3 is likely to acquire ATPase activity in a post-ER, but pre-Golgi, compartment, thus avoiding unproductive ATP hydrolysis and interference with protein folding in the ER. ER-targeted NTPDase3 may be a useful experimental tool to study the effects of ER ATP depletion on ER function under normal and stress conditions.
外核苷三磷酸二磷酸水解酶,即NTPDase1(CD39)和NTPDase3,是完整的质膜蛋白,可水解细胞外核苷酸,从而调节嘌呤能受体的功能。在分泌途径的加工过程中,外核苷酸酶的活性位点位于囊泡腔中,因此引发了一个问题,即外核苷酸酶是否会影响这些腔室中依赖ATP的过程,包括内质网(ER)中的蛋白质折叠。据报道(《生物化学杂志》(2001年)276卷,41518 - 41525页),CD39直到到达质膜才具有活性,这表明高尔基体中的终末糖基化对其活性至关重要。为了研究外核苷酸酶的亚细胞定位和激活机制,我们在COS - 1细胞中表达了人NTPDase3,并使用莫能菌素或布雷菲德菌素A阻断分泌运输,或者通过信号肽将其靶向内质网。细胞表面生物素化、对糖苷酶的敏感性以及荧光显微镜分析表明,与之前关于CD39的报道相反,NTPDase3在内质网或内质网 - 高尔基体中间腔室中变得具有催化活性,并且高尔基体中的终末糖基化对活性并非必不可少。此外,靶向内质网的NTPDase3,但不是野生型NTPDase3或靶向内质网的无活性G221A突变体,显著降低了作为报告蛋白共表达的CD39的折叠效率和向质膜的转运。这些数据表明,靶向内质网的NTPDase3显著消耗内质网中的ATP,而野生型NTPDase3可能在ER后但高尔基体前的腔室中获得ATP酶活性,从而避免了无效的ATP水解以及对内质网中蛋白质折叠的干扰。靶向内质网的NTPDase3可能是一种有用的实验工具,用于研究在正常和应激条件下内质网ATP消耗对内质网功能的影响。