The origin of complete and mosaic mutants from mutagenic treatment of single cells |
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| Authors: | A Nasim C Auerbach |
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| Affiliation: | 1. School of Life Sciences, Yunnan Normal University, Kunming, Yunnan, 650500, China;2. The Engineering Research Center of Sustainable Development and Utilization of Biomass Energy, Ministry of Education, Kunming, Yunnan, 650500, China;3. Yunnan Environmental Mutagen Society, Kunming, Yunnan, 650500, China;1. Sorbonne Université, Institut National de la Santé et de la Recherche Médicale (INSERM), “Childhood genetic disorders”, Paris, France;2. Département de Génétique Médicale, Hôpital Armand Trousseau, Assistance Publique-Hôpitaux de Paris, Paris, France;3. Service de Pédiatrie Générale, Maladies Infectieuses et Médecine Interne Pédiatrique, Centre de Référence Rhumatismes et Auto-Immunité Systémique de l''Enfant, Hôpital Robert Debré, Assistance Publique-Hôpitaux de Paris, Paris, France;4. Service de Médecine Interne, Centre Hospitalier Universitaire Pontchaillou, Rennes, France;5. Service de Médecine Interne, et Centre de Référence des Maladies Autoinflammatoires et des Amyloses Inflammatoires, Hôpital Tenon, Assistance Publique-Hôpitaux de Paris, Paris, France |
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| Abstract: | A system of colour mutation in Schizosaccharomyces pombe was used for testing current theories on the production of complete (non-sectored) mutations by mutagenic treatment of uninucleate cells. Cells of the purple adn-7 strain were exposed to UV, EMS, NMG and HA, and the frequencies of complete and mosaic forward mutations were scored at 5 antecedent loci in the adenine pathway, all of which yield white mutant cells.At equivalent values of survival or overall mutation frequency, the mutants produced by the various mutagens included different proportions of mosaics, rangin from about 905 for HA to from 13 to 48% for UV; EMS and NMG gave intermediate values, similar to those previously found for HNO2. There was no overlap in the range of mosaic production between HA and UV, and very little overlap between the other chemicals and HA on the one hand, UV on the other.Spurious mosaicism through clumping was excluded by special tests. Approximately the same proportion of mosaics was obtained whether treatment was given to growing cells, to cells in the stationary phase, or to ascospores; this shows that the contribution of already duplicated chromosomes or genes to mosaicism was negligible in these experiments.While nitrous acid has been shown to produce the same proportion of mosaics over a wide range of doses, the mutagens used in the present study yielded increasingly lower propertions of mosaics with increasing dose. Qualitatively, this trend would be expected if completes originated from mosaics in which the complementary sttrand had suffered a lethal hit, but quantatively the decrease was much too small to fit this hypothesis.In the discussion it is shown that our results are incompatible with 2 of the existing hypotheses: the master-strand hypothesis of DNA replication, and the lethal-hit hypothesis mentioned above. They are compatible with the 2 remaiining hypotheses, one of which postulates that complete and mosaic mutations arise by different molecular mechanisms, while the other assumes that mosaics are transformed into completes through repair of mismatched bases. Expected consequences of these hypotheses are open to tests, and suggestions for such tests have been put forward. |
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