Symposium No. 2: Mutagenesis. Introduction by the Chairman.

I presume I have been awarded the honor of chairing and introducing this session because I have been in mutation research for over three decades and thus can see the links between the present findings and aims in this field and those of earlier periods. It is true that my own research has been mainly concerned with chemical mutagenesis, but one of the exciting aspects of modern mutation research is the breaking down of the divisions between the induction of mutations by ionizing and non-ionizing radiations, and by various groups of chemical mutagens. We perceive, although still imperfectly, that all mutations-whatever the primary lesion in DNA-require cellular processes for their completion: repair, replication, perhaps recombination. By means of studies on mutation and antimutator genes we have come to see that the same processes play a role in the origin of spontaneous mutations, so that also the barrier between spontaneous and induced mutation is becoming tenuous. 1 expect that we shall hear more about this from DR. DRAKE. This new picture of mutzgenesis has emerged gradually during the last decade. It followed a period during which mutation research was concerned almost exclusively with the identification of the primary lesions that different mutagenic agents produce by DNA. This approach carried with it the danger of making us forget that the cell is not just a neutral container of DNA. Indeed, for a time it seemed as though mutation research had become a branch of nucleic acid chemistry. Observations that did not fit into the simple chemical scheme did turn up, but there was a tendency to brush them aside as irrelevant. This worried me a lot because it seemed so obvious to me that the process of mutagenesis, like every other biological process, must be deeply embedded in the complex biochemical pattern of cellular metabolism. However, I realize now that this onesided concentration on chemical changes in DNA was justified by its spectacular and farreaching success. Primary mutational changes can now be classified into basechanges, frameshifts and deletions, whh further subdivisions within each class. Mutagens in turn can be classified by the types of lesion they produce, and this provides a quick means of screening for potential mutagens and carcinogens in the environment. We shall hear about this from DR. AMES. Probably the greatest impact of the analysis of mutational lesions in DNA was on the fields outside mutation research. I need hardly remind you of the part played by the knowledge of molecular changes in mutant DNA in elucidating the nature of the genetic code, in establishing the colinearity of genes and polypeptides, in unravelling the mechanism of super-suppression, and in analyzing the roles played by ribosomes and transfer-RNA’s in translation.