Phenotypic lag and mutation to 6-thioguanine resistance in diploid human lymphoblasts. |
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| Authors: | W G Thilly J G Deluca H Hoppe B W Penman |
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| Affiliation: | Toxicology Group, Department of Nutrition and Food Science, Massachusetts Institute of Technology, Room E18-666, Cambridge, Mass. 02139 U.S.A. |
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| Abstract: | Mutants of a diploid human lymphoblast line resistant to 6-thioguanine (6TG) appear 6--16 generations after treatment with any of a diverse group of mutagents: methylnitrosourea (MNU), methylnitrosoguanidine (MNNG), ICR-191, 5-bromodeoxyuridine (BUdR). A hypothesis is advanced that expression of the 6-thioguanine-resistant state may require the removal of essentially all pre-existing hypoxanthine--guanine phosphoribosyl transferase (HGPRT) molecules via division, dilution, and protein turnover. Design of protocols for quantitative mutation assays requires attention to this phenomenon. |
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| Keywords: | 8 AG 8-azaguanine BUdR 5-bromodeoxyuridine HGPRT hypoxanthine—guanine phosphoribosyl transferase MNNG methylnitrosoguanidine MNU methylnitrosourea 6TG 6-thioguanine 6TG-resistant PBS phosphate-buffered saline |
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