Lundorf M D, Pedersen F S, O'Hara B, Pedersen L
Department of Molecular and Structural Biology, University of Aarhus, DK-8000 Aarhus C, Denmark.
J Virol. 1999 Apr;73(4):3169-75. doi: 10.1128/JVI.73.4.3169-3175.1999.
Pit2 is the human receptor for amphotropic murine leukemia virus (A-MuLV); the related human protein Pit1 does not support A-MuLV entry. Interestingly, chimeric proteins in which either the N-terminal or the C-terminal part of Pit2 was replaced by the Pit1 sequence all retained A-MuLV receptor function. A possible interpretation of these observations is that Pit1 harbors sequences which can specify A-MuLV receptor function when presented in a protein context other than Pit1, e.g., in Pit1-Pit2 hybrids. We reasoned that such Pit1 sequences might be identified if presented in the Neurospora crassa protein Pho-4. This protein is distantly related to Pit1 and Pit2, predicted to have a similar membrane topology with five extracellular loops, and does not support A-MuLV entry. We show here that introduction of the Pit1-specific loop 2 sequence conferred A-MuLV receptor function upon Pho-4. Therefore, we conclude that (i) a functional A-MuLV receptor can be constructed by combining sequences from two proteins each lacking A-MuLV receptor function and that (ii) a Pit1 sequence can specify A-MuLV receptor function when presented in another protein context than that provided by Pit1 itself. Previous results indicated a role of loop 4 residues in A-MuLV entry, and the presence of a Pit2-specific loop 4 sequence was found here to confer A-MuLV receptor function upon Pho-4. Moreover, the introduction of a Pit1-specific loop 4 sequence, but not of a Pit2-specific loop 4 sequence, abolished the A-MuLV receptor function of a Pho-4 chimera harboring the Pit1-specific loop 2 sequence. Together, these data suggest that residues in both loop 2 and loop 4 play a role in A-MuLV receptor function. A-MuLV is, however, not dependent on the specific Pit2 loop 2 and Pit2 loop 4 sequences for entry; rather, the role played by loops 2 and 4 in A-MuLV entry can be fulfilled by several different combinations of loop 2 and loop 4 sequences. We predict that the residues in loops 2 and 4, identified in this study as specifying A-MuLV receptor function, are to be found among those not conserved among Pho-4, Pit1, and Pit2.
Pit2是嗜双嗜性小鼠白血病病毒(A-MuLV)的人类受体;相关的人类蛋白Pit1不支持A-MuLV进入。有趣的是,Pit2的N端或C端部分被Pit1序列取代的嵌合蛋白都保留了A-MuLV受体功能。对这些观察结果的一种可能解释是,Pit1含有一些序列,当它们出现在Pit1以外的蛋白质环境中时,例如在Pit1-Pit2杂合体中,可以指定A-MuLV受体功能。我们推断,如果这些Pit1序列出现在粗糙脉孢菌蛋白Pho-4中,可能会被识别出来。这种蛋白与Pit1和Pit2有较远的亲缘关系,预计具有相似的膜拓扑结构,有五个细胞外环,并且不支持A-MuLV进入。我们在此表明,引入Pit1特异性的环2序列赋予了Pho-4 A-MuLV受体功能。因此,我们得出结论:(i)通过组合两种各自缺乏A-MuLV受体功能的蛋白质的序列,可以构建出一种功能性的A-MuLV受体;(ii)当Pit1序列出现在Pit1自身以外的另一种蛋白质环境中时,可以指定A-MuLV受体功能。先前的结果表明环4残基在A-MuLV进入中起作用,并且在此发现Pit2特异性的环4序列赋予了Pho-4 A-MuLV受体功能。此外,引入Pit1特异性的环4序列,但不引入Pit2特异性的环4序列,消除了含有Pit1特异性环2序列的Pho-4嵌合体的A-MuLV受体功能。总之,这些数据表明环2和环4中的残基在A-MuLV受体功能中都起作用。然而,A-MuLV进入并不依赖于特定的Pit2环2和Pit2环4序列;相反,环2和环4在A-MuLV进入中所起的作用可以由环2和环4序列的几种不同组合来实现。我们预测,在本研究中被确定为指定A-MuLV受体功能的环2和环4中的残基,将在Pho-4、Pit1和Pit2中不保守的那些残基中被发现。