Expression of a novel high affinity purine base transport system in mutant mouse S49 cells does not require a functional nucleoside transporter.

J. Beck, Buddy Ullman

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1 Citation (Scopus)

Abstract

A novel type of somatic mutation that causes the expression of a high affinity purine base permease has been inserted into murine S49 lymphoma cells that are deficient in nucleoside transport. Two classes of mutants expressing this nucleobase permease were generated. The first, as exemplified by the AE1HADPAB2 cell line, possesses 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, possesses an augmented capability to translocate low levels of hypoxanthine and guanine, but not adenine. Neither the AE1HADPAB2 nor the AE1HADPAB5 cells can transport nucleosides suggesting that the expression of the high affinity base transporter did not revert the mutation in the nucleoside transport system. 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.

Original languageEnglish (US)
Pages (from-to)525-532
Number of pages8
JournalAdvances in Experimental Medicine and Biology
Volume253 B
StatePublished - 1989

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Nucleoside Transport Proteins
Nucleosides
Hypoxanthine
Membrane Transport Proteins
Guanine
Adenine
Cells
Cell Line
Mutation
Genetic Loci
Fusion reactions
Genes
purine
Lymphoma
Clone Cells
Gene Expression

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

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title = "Expression of a novel high affinity purine base transport system in mutant mouse S49 cells does not require a functional nucleoside transporter.",
abstract = "A novel type of somatic mutation that causes the expression of a high affinity purine base permease has been inserted into murine S49 lymphoma cells that are deficient in nucleoside transport. Two classes of mutants expressing this nucleobase permease were generated. The first, as exemplified by the AE1HADPAB2 cell line, possesses 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, possesses an augmented capability to translocate low levels of hypoxanthine and guanine, but not adenine. Neither the AE1HADPAB2 nor the AE1HADPAB5 cells can transport nucleosides suggesting that the expression of the high affinity base transporter did not revert the mutation in the nucleoside transport system. 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.",
author = "J. Beck and Buddy Ullman",
year = "1989",
language = "English (US)",
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journal = "Advances in Experimental Medicine and Biology",
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T1 - Expression of a novel high affinity purine base transport system in mutant mouse S49 cells does not require a functional nucleoside transporter.

AU - Beck, J.

AU - Ullman, Buddy

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N2 - A novel type of somatic mutation that causes the expression of a high affinity purine base permease has been inserted into murine S49 lymphoma cells that are deficient in nucleoside transport. Two classes of mutants expressing this nucleobase permease were generated. The first, as exemplified by the AE1HADPAB2 cell line, possesses 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, possesses an augmented capability to translocate low levels of hypoxanthine and guanine, but not adenine. Neither the AE1HADPAB2 nor the AE1HADPAB5 cells can transport nucleosides suggesting that the expression of the high affinity base transporter did not revert the mutation in the nucleoside transport system. 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.

AB - A novel type of somatic mutation that causes the expression of a high affinity purine base permease has been inserted into murine S49 lymphoma cells that are deficient in nucleoside transport. Two classes of mutants expressing this nucleobase permease were generated. The first, as exemplified by the AE1HADPAB2 cell line, possesses 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, possesses an augmented capability to translocate low levels of hypoxanthine and guanine, but not adenine. Neither the AE1HADPAB2 nor the AE1HADPAB5 cells can transport nucleosides suggesting that the expression of the high affinity base transporter did not revert the mutation in the nucleoside transport system. 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.

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