Ugolev Yelena, Berdichevsky Yevgeny, Weinbaum Carolyn, Pick Edgar
Julius Friedrich Cohnheim-Minerva Center for Phagocyte Research and the Ela Kodesz Institute of Host Defense against Infectious Diseases, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel.
J Biol Chem. 2008 Aug 8;283(32):22257-71. doi: 10.1074/jbc.M800734200. Epub 2008 May 27.
Rac plays a pivotal role in the assembly of the superoxide-generating NADPH oxidase of phagocytes. In resting cells, Rac is found in the cytosol in complex with Rho GDP dissociation inhibitor (RhoGDI). NADPH oxidase assembly involves dissociation of the Rac.RhoGDI complex and translocation of Rac to the membrane. We reported that liposomes containing high concentrations of monovalent anionic phospholipids cause Rac.RhoGDI complex dissociation ( Ugolev, Y., Molshanski-Mor, S., Weinbaum, C., and Pick, E. (2006) J. Biol. Chem. 281, 19204-19219 ). We now designed an in vitro model mimicking membrane phospholipid remodeling during phagocyte stimulation in vivo. We showed that liposomes of "resting cell membrane" composition (less than 20 mol % monovalent anionic phospholipids), supplemented with 1 mol % of polyvalent anionic phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4,5)P(3)) in conjunction with constitutively active forms of the guanine nucleotide exchange factors (GEFs) for Rac, Trio, or Tiam1 and a non-hydrolyzable GTP analogue, cause dissociation of Rac1(GDP).RhoGDI complexes, GDP to GTP exchange on Rac1, and binding of Rac1(GTP) to the liposomes. Complexes were not dissociated in the absence of GEF and GTP, and optimal dissociation required the presence of PtdIns(3,4,5)P(3) in the liposomes. Dissociation of Rac1(GDP).RhoGDI complexes was correlated with the affinity of particular GEF constructs, via the N-terminal pleckstrin homology domain, for PtdIns(3,4,5)P(3) and involved GEF-mediated GDP to GTP exchange on Rac1. Phagocyte membranes enriched in PtdIns(3,4,5)P(3) responded by NADPH oxidase activation upon exposure in vitro to Rac1(GDP).RhoGDI complexes, p67(phox), GTP, and Rac GEF constructs with affinity for PtdIns(3,4,5)P(3) at a level superior to that of native membranes.
Rac在吞噬细胞产生超氧化物的NADPH氧化酶组装过程中起关键作用。在静息细胞中,Rac存在于胞质溶胶中,与Rho GDP解离抑制剂(RhoGDI)形成复合物。NADPH氧化酶组装涉及Rac.RhoGDI复合物的解离以及Rac向膜的转位。我们报道过,含有高浓度单价阴离子磷脂的脂质体可导致Rac.RhoGDI复合物解离(乌戈列夫,Y.,莫尔尚斯基 - 莫尔,S.,温鲍姆,C.,以及皮克,E.(2006年)《生物化学杂志》281卷,19204 - 19219页)。我们现在设计了一个体外模型,模拟体内吞噬细胞刺激过程中的膜磷脂重塑。我们发现,“静息细胞膜”组成的脂质体(单价阴离子磷脂含量低于20摩尔%),补充1摩尔%的多价阴离子磷脂酰肌醇3,4,5 - 三磷酸(PtdIns(3,4,5)P(3)),并结合Rac的鸟嘌呤核苷酸交换因子(GEF)组成型活性形式Trio或Tiam1以及一种不可水解的GTP类似物,可导致Rac1(GDP).RhoGDI复合物解离、Rac1上的GDP与GTP交换以及Rac1(GTP)与脂质体结合。在没有GEF和GTP的情况下复合物不会解离,并且最佳解离需要脂质体中存在PtdIns(3,4,5)P(3)。Rac1(GDP).RhoGDI复合物的解离与特定GEF构建体通过N端普列克底物蛋白同源结构域对PtdIns(3,4,5)P(3)的亲和力相关,并且涉及GEF介导的Rac1上的GDP与GTP交换。富含PtdIns(3,4,5)P(3)的吞噬细胞膜在体外暴露于Rac1(GDP).RhoGDI复合物、p67(phox)、GTP以及对PtdIns(3,4,5)P(3)亲和力高于天然膜的Rac GEF构建体时,会通过NADPH氧化酶激活做出反应。