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野生型和突变型光感受器外周蛋白/视网膜变性慢病毒在马-达二氏犬肾细胞中的异源表达:融合功能评估

Heterologous expression of WT and mutant photoreceptor peripherin/rds in Madin Darby canine kidney cells: an assessment of fusogenic function.

作者信息

Stefano Frank P, Krouse Jennifer, Marta Peter, Boesze-Battaglia Kathleen

机构信息

Department of Molecular Biology, University of Medicine and Dentistry of New Jersey-SOM, 2 Medical Center Drive, Stratford, NJ 08084, U.S.A.

出版信息

Exp Eye Res. 2002 Feb;74(2):267-83. doi: 10.1006/exer.2001.1119.

Abstract

Peripherin/rds is proposed to function as a fusion protein within the rod outer segment and a fusion domain has been mapped to amino acids 311-325 within the C-terminus. To map regions within peripherin/rds required for membrane fusion a series of C-terminal mutants was analyzed. Madin Darby canine kidney cells were transiently transfected with an Xpress or FLAG epitope tagged peripherin/rds (wt) and three mutants of peripherin/rds. The mutants selected were a P296T mutant (replacement of the proline at position 296 with a threonine) and two C-terminal deletion mutants (one lacking the terminal 10 amino acids, Delta10 and one lacking the terminal 50 amino acids, Delta50). The wt protein, the P296T and Delta10 mutants were detected on SDS-PAGE as 84 kDa dimers, that resolved into 38-42 kDa monomers under reducing conditions. The Delta50 mutant showed a slightly increased mobility. The cellular localization of mutants differed from that of wt peripherin/rds. The wt Xpress-human and wt FLAG-bovine peripherin/rds were localized to both intracellular and plasma membranes. In contrast, the C-terminal deletion mutants were localized only to the intracellular membrane. The P296T mutant presented a still different pattern: initially the protein localized to intracellular membranes. Upon confluence, however, the localization appeared to become predominantly plasma membrane. To assess the fusion activity of the proteins, the cell membranes were fractionated using sucrose density gradient centrifugation and the various fractions identified based on immunoreactivity in Western blot analysis with Golgi (anti-rab 6) or plasma membrane (anti-ZO-3) specific marker proteins. All membrane fractions were assayed for fusion with ROS plasma membrane vesicles. The plasma membrane enriched fractions (isolated at densities of 1.08 and 1.125 g ml(-1)) containing tagged peripherin/rds and the Delta10 mutant promoted membrane fusion with ROS plasma membrane vesicles. In contrast, fusion was not detected with plasma membrane vesicles from mock-transfected cells or the Delta50 peripherin/rds deletion mutant. Fusion was enhanced in a less dense fraction enriched in the P296T mutant (isolated from the 1.04/1.02 interface) relative to wt. Fusion was dependent on the presence of peripherin/rds in the membranes and could be inhibited with trypsinolysis and competition studies with the bovine fusion peptide, PP-5. Peptide competition suggests that the fusion domain of human peripherin/rds is most likely identical to that characterized in bovine and corresponds to amino acid residues 312-326. The C-terminal deletion mutants have allowed us to predict the minimal region of the C-terminus necessary for fusion to include residues starting at number 335. In addition a second region important in the formation of a fusion competent peripherin/rds has been mapped to a region upstream of the fusion peptide domain.

摘要

外周蛋白/视网膜变性慢病毒(Peripherin/rds)被认为在视杆细胞外段中作为融合蛋白发挥作用,并且已经确定一个融合结构域位于C末端的第311 - 325个氨基酸处。为了确定外周蛋白/视网膜变性慢病毒中膜融合所需的区域,对一系列C末端突变体进行了分析。将表达Xpress或FLAG表位标签的外周蛋白/视网膜变性慢病毒(野生型)以及外周蛋白/视网膜变性慢病毒的三个突变体瞬时转染到Madin Darby犬肾细胞中。选择的突变体是P296T突变体(将第296位的脯氨酸替换为苏氨酸)和两个C末端缺失突变体(一个缺失末端10个氨基酸,Delta10;另一个缺失末端50个氨基酸,Delta50)。野生型蛋白、P296T和Delta10突变体在SDS - PAGE上被检测为84 kDa的二聚体,在还原条件下分解为38 - 42 kDa的单体。Delta50突变体显示出迁移率略有增加。突变体的细胞定位与野生型外周蛋白/视网膜变性慢病毒不同。野生型Xpress - 人外周蛋白/视网膜变性慢病毒和野生型FLAG - 牛外周蛋白/视网膜变性慢病毒定位于细胞内和质膜。相比之下,C末端缺失突变体仅定位于细胞内膜。P296T突变体呈现出不同的模式:最初该蛋白定位于细胞内膜。然而,汇合后,定位似乎主要变为质膜。为了评估这些蛋白的融合活性,使用蔗糖密度梯度离心法分离细胞膜,并根据用高尔基体(抗rab 6)或质膜(抗ZO - 3)特异性标记蛋白进行的蛋白质印迹分析中的免疫反应性来鉴定各个组分。对所有膜组分进行与视杆细胞外段质膜囊泡融合的检测。含有标记的外周蛋白/视网膜变性慢病毒和Delta10突变体的富含质膜的组分(在密度为1.08和1.125 g/ml(-1)处分离)促进了与视杆细胞外段质膜囊泡的膜融合。相比之下,未检测到与 mock - 转染细胞的质膜囊泡或Delta50外周蛋白/视网膜变性慢病毒缺失突变体的融合。相对于野生型,在富含P296T突变体的密度较小的组分(从1.04/1.02界面分离)中融合增强。融合依赖于膜中外周蛋白/视网膜变性慢病毒的存在,并且可以通过胰蛋白酶消化和与牛融合肽PP - 5的竞争研究来抑制。肽竞争表明人外周蛋白/视网膜变性慢病毒的融合结构域很可能与牛的相同,对应于氨基酸残基312 - 326。C末端缺失突变体使我们能够预测融合所需的C末端的最小区域,包括从第335位开始的残基。此外,在形成具有融合能力的外周蛋白/视网膜变性慢病毒中起重要作用的第二个区域已被定位到融合肽结构域上游的一个区域。

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