Tests for induction of dominant-lethal mutations and heritable translocations with tetrahydrocannabinol in male mice.
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W M Generoso
Publications and source records attributed to W M Generoso.
Tissue-specific variation in repair activity for 3-methyladenine in DNA in two stocks of mice.
Two stocks of mice, hybrid (C3H X 101)F1 and inbred SEC/R1, were compared for 3-methyladenine-DNA N-glycosylase activity which is involved in removal of 3-methyladenine, 7-methylguanine and some other N-methylpurines in DNA, in cell-free extracts of different tissues. Based on activity measured both per unit weight of tissue and per mass DNA, there is a significant organ-specific and stock-specific difference in N-glycosylase activity over a range of 0.5-8.7 fmoles of 3-methyladenine released per h at 37 degrees C per micrograms DNA of tissue extract. On a per cell basis, the repair activity for 3-methyladenine is the highest in stomach in both stocks. The tissue can be arranged in order of decreasing activity of glycolytic removal as stomach greater than kidney greater than lung greater than liver greater than spleen greater than brain greater than ovary for SEC/R1 mice and stomach greater than kidney greater than ovary greater than spleen, lung and brain greater than liver for the hybrid mice. For all tissues except ovary, SEC/R1 mice have 1.5-4-fold higher specific N-glycosylase activity than (C3H X 101)F1 mice. In contrast, the ovary of SEC/R1 stock has about half as much enzyme activity as that of the hybrid stock.
Adenine↗
Induced mouse chromosomal rearrangements as tools for identifying critical developmental genes and pathways.
Due to the rapid advances that have been made in molecular and genetic technology during the past decade, the genes associated with a large number of human hereditary diseases have been isolated and analyzed in detail. These cloned genes provide new tools for research geared toward a better understanding of normal human development, and also of the many ways that basic, essential morphologic pathways can be disturbed. Chromosomal rearrangements, especially deletions and translocations, have been especially beneficial in the mapping and isolation of human disease genes because of their visibility on both the cytogenetic and molecular levels. However, these useful types of mutations occur with low frequency in the human population. Chromosomal rearrangements can be induced relatively easily in mice, and several large, independent collections of translocation and deletion mutants have been generated in the course of risk-assessment and mutagenesis studies over the past several decades. Combined with new molecular technologies, these collections of mutant animals provide a means of gaining ready access to genes associated with developmental defects including craniofacial abnormalities, hydrocephaly, skeletal deformities, and complex neurologic disorders. As an illustration of this approach, we briefly review our progress in the study of three mutations associated with defects in palate development, juvenile growth, fitness and sterility, and neurologic development in mice, respectively.
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