TY - JOUR
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, B.
N1 - Copyright:
This record is sourced from MEDLINE/PubMed, a database of the U.S. National Library of Medicine
PY - 1989
Y1 - 1989
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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U2 - 10.1007/978-1-4684-5676-9_78
DO - 10.1007/978-1-4684-5676-9_78
M3 - Article
C2 - 2610142
AN - SCOPUS:0024780138
SN - 0065-2598
VL - 253 B
SP - 525
EP - 532
JO - Advances in experimental medicine and biology
JF - Advances in experimental medicine and biology
ER -