Smith J D, Myers N B, Gorka J, Hansen T H
Department of Genetics, Washington University School of Medicine, St. Louis, Missouri 63110.
J Exp Med. 1993 Dec 1;178(6):2035-46. doi: 10.1084/jem.178.6.2035.
To characterize the process of class I assembly and maturation, we have studied the Ld molecule of the mouse. Previous studies have shown that a significant proportion of intracellular and surface Ld molecules can be detected in an alternative conformation designated Ldalt1. Nascent Ldalt molecules are non-peptide ligand associated and are weakly associated with beta 2-microglobulin (beta 2m). Unexpectedly, when monoclonal antibodies were added directly to the lysis buffer, significant amounts of Ldalt/beta 2m heterodimer were detected, suggesting that beta 2m association is not necessarily sufficient to induce Ld conformation. By contrast, addition of peptide to cell lysates rapidly induced the folding of beta 2m-associated Ldalt to conformed Ld. Furthermore, the time course and dynamics of this conversion correlated precisely with peptide binding to Ld. The precursor-product relationship of Ldalt and conformed Ld was also visualized in vivo by pulse-chase analysis of BALB/c splenocytes. To investigate the factors that regulate intracellular transport of class I molecules, expression of Ld was studied in the peptide transport-deficient cell line, RMA.S-Ld, and in beta 2m-/- splenocytes. In contrast to wild-type cell lines, both Ldalt and conformed Ld are poorly expressed at the cell surface of RMA.S-Ld and beta 2m-/- splenocytes. Therefore, surface expression of Ldalt is dependent upon the concomitant expression of conformed Ld molecules. To determine whether surface Ldalt molecules can result from melting of conformed Ld molecules, surface Ld molecules were loaded with several different known Ld peptide ligands. Complexes of Ld with different ligands were found to have dramatically disparate surface half-lives. Importantly, the Ld peptide complexes that turned over the most rapidly resulted in the most gain in surface Ldalt, implying that peptide dissociation can induce the accumulation of nonconformed Ld heavy chains at the cell surface.
为了描述I类分子组装和成熟的过程,我们研究了小鼠的Ld分子。先前的研究表明,在一种称为Ldalt1的替代构象中可以检测到相当比例的细胞内和表面Ld分子。新生的Ldalt分子不与肽配体结合,并且与β2-微球蛋白(β2m)弱结合。出乎意料的是,当将单克隆抗体直接添加到裂解缓冲液中时,检测到大量的Ldalt/β2m异二聚体,这表明β2m结合不一定足以诱导Ld构象。相比之下,向细胞裂解物中添加肽会迅速诱导与β2m结合的Ldalt折叠成构象正确的Ld。此外,这种转化的时间进程和动力学与肽与Ld的结合精确相关。通过对BALB/c脾细胞进行脉冲追踪分析,还在体内观察到了Ldalt和构象正确的Ld之间的前体-产物关系。为了研究调节I类分子细胞内运输的因素,在肽转运缺陷细胞系RMA.S-Ld和β2m-/-脾细胞中研究了Ld的表达。与野生型细胞系相比,Ldalt和构象正确的Ld在RMA.S-Ld和β2m-/-脾细胞的细胞表面均表达不佳。因此,Ldalt的表面表达取决于构象正确的Ld分子的同时表达。为了确定表面Ldalt分子是否可能由构象正确的Ld分子的解链产生,用几种不同的已知Ld肽配体加载表面Ld分子。发现Ld与不同配体的复合物具有截然不同的表面半衰期。重要的是,周转最快的Ld肽复合物导致表面Ldalt增加最多,这意味着肽解离可以诱导细胞表面未折叠的Ld重链积累。