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首页> 外文期刊>Molecular and Cellular Biology >Expression of the high-affinity purine nucleobase transporter in mutant mouse S49 cells does not require a functional wild-type nucleoside-nucleobase transporter.
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Expression of the high-affinity purine nucleobase transporter in mutant mouse S49 cells does not require a functional wild-type nucleoside-nucleobase transporter.

机译：高亲和力嘌呤核苷碱基转运蛋白在突变小鼠S49细胞中的表达不需要功能性野生型核苷-核苷碱基转运蛋白。

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摘要

A novel type of somatic mutation that causes the expression of a high-affinity purine base permease (B. Aronow, D. Toll, J. Patrick, P. Hollingsworth, K. McCartan, and B. Ullmann, Mol. Cell Biol. 6:2957-2962, 1986) has been inserted into nucleoside transport-deficient S49 cells. Two classes of mutants expressing this nucleobase permease were generated. The first, as exemplified by the AE1HADPAB2 cell line, possessed an augmented capacity to transport low concentrations of the three purine bases, hypoxanthine, guanine, and adenine. The second class of mutants, as typified by the AE1HADPAB5 clone, possessed an augmented capability to translocate low levels of hypoxanthine and guanine, but not adenine. Neither the AE1HADPAB2 nor the AE1HADPAB5 cells could transport nucleosides, suggesting that the expression of the high-affinity base transporter did not reverse the mutation in the nucleoside transport system. The transport of purine bases by both AE1HADPAB2 and AE1HADPAB5 cells was much less sensitive than that by wild-type cells to inhibition by dipyridamole, 4-nitrobenzylthionosine, and N-ethylmaleimide, potent inhibitors of nucleoside and nucleobase transport in wild-type S49 cells. Fusion of the AE1HADPAB2 and AE1HADPAB5 cell lines with wild-type cells indicated that the expression of the high-affinity base transporter behaved in a dominant fashion, while the nucleoside transport deficiency was a recessive trait. These data suggest that the high-affinity purine base transporter of mutant cells and the nucleoside transport function of wild-type cells are products of different genes and that expression of the former probably requires the unmasking or alteration of a specific genetic locus that is silent or different in wild-type cells.
机译：一种新型的体细胞突变，引起高亲和性嘌呤碱基通透酶的表达（B. Aronow，D。Toll，J。Patrick，P。Hollingsworth，K。McCartan，以及B. Ullmann，Mol。Cell Biol。6 ：2957-2962，1986）已被插入到缺乏核苷转运的S49细胞中。产生了两类表达该核碱基通透酶的突变体。以AE1HADPAB2细胞系为例，第一个具有增强的能力，可以运输低浓度的三种嘌呤碱基，次黄嘌呤，鸟嘌呤和腺嘌呤。以AE1HADPAB5克隆为代表的第二类突变体具有增强的转运低水平次黄嘌呤和鸟嘌呤而不是腺嘌呤的能力。 AE1HADPAB2和AE1HADPAB5细胞均不能转运核苷，这表明高亲和力碱基转运蛋白的表达不能逆转核苷转运系统中的突变。 AE1HADPAB2和AE1HADPAB5细胞对嘌呤碱基的转运对野生型S49细胞中核苷和核碱基转运的有效抑制剂双嘧达莫，4-硝基苄基硫代腺苷和N-乙基马来酰亚胺的抑制作用远不如野生型细胞敏感。 AE1HADPAB2和AE1HADPAB5细胞系与野生型细胞的融合表明，高亲和力碱基转运蛋白的表达以显性方式表现，而核苷转运缺陷是一种隐性性状。这些数据表明，突变细胞的高亲和力嘌呤碱基转运蛋白和野生型细胞的核苷转运功能是不同基因的产物，而前者的表达可能需要揭示或改变沉默或突变的特定基因座。在野生型细胞中有所不同。

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