Jascur T, Goldenberg D P, Vestweber D, Schatz G
Biocenter, University of Basel, Switzerland.
J Biol Chem. 1992 Jul 5;267(19):13636-41.
We have constructed a chimeric mitochondrial precursor protein consisting of a mutant bovine pancreatic trypsin inhibitor coupled to the C terminus of a purified artificial precursor protein. This construct fails to complete its import into isolated mitochondria and becomes stuck across sites of close contact between the two mitochondrial membranes. When the mitochondria are then depleted of ATP and the intramolecular disulfide bridges of the trypsin inhibitor are cleaved by dithiothreitol, the trypsin inhibitor moiety is transported across the outer membrane into the intermembrane space. This translocation intermediate can be chased across the inner membrane by restoring the ATP levels in the matrix. These results show that translocation of pancreatic trypsin inhibitor across a biological membrane is prevented by its intramolecular disulfide bridges, that import into the matrix involves two distinct translocation system operating in tandem, and that ATP is required for protein translocation across the inner but not the outer membrane.
我们构建了一种嵌合线粒体前体蛋白,它由与纯化的人工前体蛋白C末端相连的突变型牛胰蛋白酶抑制剂组成。这种构建体无法完成其导入分离线粒体的过程,并被困在两个线粒体膜紧密接触的部位。当线粒体随后耗尽ATP且胰蛋白酶抑制剂的分子内二硫键被二硫苏糖醇裂解时,胰蛋白酶抑制剂部分穿过外膜进入膜间隙。通过恢复基质中的ATP水平,这种易位中间体可以被转运穿过内膜。这些结果表明,胰蛋白酶抑制剂通过其分子内二硫键阻止了其跨生物膜的易位,导入基质涉及两个串联运行的不同易位系统,并且蛋白质跨内膜易位需要ATP,但跨外膜则不需要。