Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00492 (hypoxanthine-guanine phosphoribosyltransferase)
 2,385 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have previously shown that descendants of CHO-derived hprt or aprt mutants induced by ethyl methanesulphonate usually undergo a rapid loss of the mutant phenotype during the 10 generations or so of culture in non-selective medium immediately following mutagenesis (Bradley, 1980; Bradley and Laviolette, 1989). We now present an analysis of several mutants and their descendants which have lost the mutant phenotype, or 'reversed'. The drug-resistance properties of reversed cells were generally intermediate between W.T. and mutant, and message level and enzyme-specific activity were also intermediate, correlating with the phenotype. Although this was consistent with a model of inactivation-reactivation of the target gene to explain the reversal phenomenon, the model was ruled out by Northern blot analysis of several induced mutants, which showed no correlation between level of message and tendency of the mutant to lose its phenotype. Karyotype analysis showed that three out of four reversed lines were near-tetraploid and the fourth had a substantial proportion of near-tetraploid cells. This suggests cell fusion between a mutant and a W.T. cell may explain the phenomenon. A prediction of this model, namely that mutagen treatment increases cell hybrid formation, was tested and found to be true.
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PMID:Phenotype reversal in induced mutants of CHO cells: analysis of the reversed cell lines. 206 28

We have analysed the recovery of individual CHO-derived mutants during the generations immediately following their induction. This characteristic, which we call persistence, was measured by propagating mutagenized cultures in non-selective medium after subdivision into many very small populations, each containing either zero or one mutant. The recovery of most hypoxanthine phosphoribosyltransferase (hprt)-deficient mutants induced by ethyl methanesulphonate was low, and we have previously shown that this was usually due to an apparent rapid loss of the mutant phenotype with continued culture in non-selective medium (Bradley, 1980). A minority of about 15% manifest high persistence. We now show that most adenine phosphoribosyltransferase (aprt)-deficient mutants and some ouabain-resistant mutants had low persistence. Mutants induced by UV irradiation also generally exhibited low persistence but those induced by X-irradiation had significantly higher persistence than what was seen among EMS-induced mutants. Among various sublines of CHO cells which were tested for persistence of induced mutants, only one group consistently yielded mutants of high persistence. These were lines which carried glucose-6-phosphate dehydrogenase mutations which themselves had been originally induced by EMS.
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PMID:Low persistence of the induced mutant phenotype in Chinese hamster cells. 253 33

Hypoxanthine phosphoribosyltransferase deficient mutants of Chinese hamster ovary cells induced by ethyl methanesulfonate usually do not maintain their phenotype during growth in non-selective medium immediately following the induction. This phenomenon, called poor "persistence" of the induced mutation, is in most cases unrelated to growth rate but results from establishment of contact with wild type cells (Bradley, W. E. C. Exp. Cell Res., 129: 251, 1980). We report here that 12-O-tetradecanoylphorbol-13-acetate, a strong tumor promoter, increases the persistence of these mutants.
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PMID:Increased persistence of induced mutants of Chinese hamster cells by 12-O-tetradecanoylphorbol-13-acetate. 394 68