Section I Reviews.- 1 Relationship Between Repair Processes and Mutation Induction in Bacteria.- 2 Role of Cellular Systems in Modifying the Response to Chemical Mutagens.- 3 DNA Repair Pathways.- Section II Lower Eukaryotes.- A. Neurospora crassa.- 4 Mutagen-Sensitive Mutants in Neurospora.- 5 Nucleases and Their Control in Wild-Type and nuh Mutants of Neurospora.- 6 Mutation-Induction in Repair-Deficient Strains of Neurospora.- B. Saccharomyces cerevisiae.- 7 Genetic and Physiological Factors Affecting Repair and Mutagenesis in Yeast.- 8 Molecular Mechanism of Pyrimidine Dimer Excision in Saccharomyces cerevisiae. I. Studies with Intact Cells and Cell-Free Systems.- 9 Genetic Analysis of Error Prone Repair Systems in Saccharomyces cerevisiae.- 10 DNA Repair and Mutagen Interaction in Saccharomyces: Theoretical Considerations.- 11 Repair and Mutagenesis in Lower Eukaryotes: A Summary and Perspective.- Section III Drosophila.- 12 Isolation and Characterization of Repair-Deficient Mutants of Drosophila melanogaster.- 13 Effects of Recombination-Deficient and Repair-Deficient Loci on Meiotic and Mitotic Chromosomes Behavior in Drosophila melanogaster.- 14 Biochemical Characterization of Repair-Deficient Mutants of Drosophila.- 15 Mutation Induction in Repair-Deficient Strains of Drosophila.- 16 Repair and Mutagenesis in Drosophila: A Summary and Perspective.- Section IV Mammalian Somatic Cells.- 17 Relationship of DNA Lesions and Their Repair to Chromosomal Aberration Production.- 18 Relationship of DNA Repair and Chromosome Aberrations to Potentially Lethal Damage Repair in X-irradiated Mammalian Cells.- 19 Chromosome Aberration Formation and Sister Chromatid Exchange in Relation to DNA Repair in Human Cells.- 20 DNA Repair Process Can Alter the Frequency of Mutations Induced in Diploid Human Cells.- 21 Ultraviolet Light Induction of Diphtheria Toxin-Resistant Mutations in Normal and DNA Repair-Deficient Human and Chinese Hamster Fibroblasts.- 22 Mutation Induction in a Radiation-Sensitive Variant of Mammalian Cells.- 23 Repair of Human DNA in Molecules that Replicate or Remain Unreplicated Following Ultraviolet Irradiation.- 24 DNA Repair in Nuclei Isolated from HeLa Cells.- 25 Repair and Induction of Chromosome Aberrations and Point Mutations in Mammalian Somatic Cells: A Summary and Perspective.- Section V Mouse Germ Cells.- 26 Relationship Between Unscheduled DNA Synthesis and Mutation Induction in Male Mice.- 27 Radiation- and Drug-Induced DNA Repair in Mammalian Oocytes and Embryos.- 28 Repair in Fertilized Eggs of Mice and its Role in the Production of Chromosomal Aberrations.- 29 Repair and Mutation Induction in Mouse Germ Cells: A Summary and Some Thoughts.- Section VI Relevance to Human Health Hazard Assessment.- 30 The Chromosome-Breakage Syndromes: Different Genes, Different Treatments, Different Cancers.- 31 Summary and Perspective: Relevance to Human Health Hazard Assessment.- Contributors.
Not many years ago most discussion of mutation induction by physical and chemical agents concentrated on the initial lesions induced in the DNA with the implicit assumption that once the lesions were made they were converted almost automatically to mutations by relatively simple processes associated with DNA replication. The discovery of a variety of enzymatic processes that can repair these lesions, the great increase in our understanding of the molecular steps involved in repair, replication, and recombination, and the increasing availability of cells with genetic defects in these pro cesses have led to the realization that mutation induction is a far more complex process than we originally thought. Repair systems can remove lesions before they can be converted to mutation, they can also convert initial lesions to secondary ones that are them selves mutagenic, and they can remove potentially lethal lesions at the expense of making mutations. The error-avoiding systems asso ciated with replication are themselves complex and may be caused to make mistakes in various ways. These different pathways for mutation production and mutation avoidance are still being worked out in prokaryotes and are less well understood in eukaryotes. This symposium shows, however, that very encouraging progress has been made in the last several years, and the progress is now accelerating.
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