Abstract
We isolated three adenine auxotrophic mutants {Ade 1-3) of mouse FM3A cells deficient in aminoimidazolecarboxamide riboside (AICAR) transformylase. Ade 1 and Ade 2 also lacked inosinicase activity. Ade 2 and Ade 3 complemented in cell-cell hybrids, although Ade 1 did not either of them. An intermediate AICAR was found to accumulate in all the mutants indicating that earlier steps than that of formylation of AICAR in the purine biosynthetic pathway seem normal. Primary and secondary transformants were isolated from Ade 2 and Ade 3 using human chromosome-mediated gene transfer. All the transformants tested were found to produce both human-type AICAR transformylase and inosinicase. Unexpectedly, human DNA intergrated in the host genome of the certain primary transformant was reduced to as little is several hundred kilobase pairs in length. When digested with certain restriction endonucleases, identical human DNA bands as probed with a human Alu sequence were detected in the transformants of Ade 2 and Ade 3. Since only human chromosome 2 was enough to rescue the genetic defects in the three mutants, these mutants seem to have arisen by a mutation in the AICAR transformylase gene or its adjacent gene.
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Ayusawa, D., Shiaizu, K., Yameuchi, M. et al. 5 TWO TYPES OF MOUSE FM3A CELL MUTANTS DEFICIENT IN AMINOIMIDAZOLECAROXAMIDE RIBOTIDE TRANSFORMYLASE AND THEIR TRANSFORMANTS ISOLATED BY CHROMOSOME-MEDIATED GENE TRANSFER. Pediatr Res 24, 112 (1988). https://doi.org/10.1203/00006450-198807000-00029
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DOI: https://doi.org/10.1203/00006450-198807000-00029