Chromosome changes in 6-TG-resistant mutant strains derived from a karyotypically stable human line, C32.
Karyotypes of the human C32r16 line and its HPRT-mutant derivatives were compared. All three HPRT-mutant strains (TG-A, TG-E1, and TG-E2) studied were hypotetraploid and arose by genomic duplication. TG-A and TG-E had distinct karyotypes, reflecting their independent clonal origins. Both TG-E1 and TG-E2 were similar karyotypically, except that TG-E2 differed from TG-E1 by the presence of two new sets of balanced translocations and a significantly higher number of new markers, viz., 24 new markers in 14 TG-E2 cells as compared to 2 new markers in 13 TG-E1 cells. Comparison of the hypothetical 2s karyotype of C32r16 with the modal karyotypes of the mutants revealed (1) that chromosome changes occurred more frequently among marker chromosomes (57.1%) than among normal chromosomes (18.1%) and also more frequently among tetrasomic (28.6%) than among disomic (3.3%) normal chromosomes, and (2) that one member of a group of paired marker chromosomes tended to be eliminated very frequently, whereas disomic normal chromosomes retained their disomic condition. Chromosome 7 was involved in the formation of new marker chromosomes twice as much as any other chromosome, and even increased to pentasomy in TG-E1. Chromosome changes associated with 6-thioguanine treatment are briefly discussed.
D002460:Cell Line; D002871:Chromosome Banding; D002877:Chromosomes, Human / Q000648:ultrastructure*; D004351:Drug Resistance; D006801:Humans; D007041:Hypoxanthine Phosphoribosyltransferase / Q000235:genetics; D007621:Karyotyping; D008545:Melanoma / Q000235:genetics*; D009154:Mutation; D013866:Thioguanine / Q000633:toxicity
D007041:Hypoxanthine Phosphoribosyltransferase; D013866:Thioguanine