Abstract
We isolated three adenine auxotrophic mutants (Adel, Ade2 and Ade3) of mouse FM3A cells deficient in 5-aminoimidazole-4-carboxamide ribotide transformylase (EC 2.1.2.3) activity. Adel and Ade3 but not Adel also lacked inosinicase (EC 3.5.4.10) activity. While Ade2 and Ade3 complemented each other, Adel complemented neither Ade2 nor Ade3, suggesting that two complementation groups exist in these mutants. We introduced human genes into the Ade2 and Ade3 cells by chromosome-mediated gene transfer. All the transformants tested were found to produce the human transformylase and inosinicase, and identical DNA bands containing human Alu sequences were detected in the transformants of Ade2 and Ade3. These mutants seem to have arisen by mutation in the same gene or adjacent genes, since only human chromosome 2 was capable of rescuing the genetic defects in all these mutants.
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Yamauchi, M., Ayusawa, D., Shimizu, K. et al. Two types of mouse FM3A cell mutants deficient in 5-aminoimidazole-4-carboxamide ribonucleotide transformylase and their transformants isolated by human chromosome-mediated gene transfer. Somat Cell Mol Genet 15, 39–48 (1989). https://doi.org/10.1007/BF01534668
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DOI: https://doi.org/10.1007/BF01534668