Advances in Virus Research by Kenneth M. Smith and Max A. Lauffer (Eds.)

By Kenneth M. Smith and Max A. Lauffer (Eds.)

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The assumption that a single event results in a mutation is expressed by the equation m = 1- e-rkt in which rri is the fraction of mutants in the total population and r is the fraction of events which arc mutating events. When T is small in relation to Ict, m becomes approximately equal to rkt. The fraction of the total population which can be detected as mutants is that fraction, M , which has been mutated but not killed. Thus, A4 = ms = rkte& and from which it can be seen that M will have a maximum value when k t is equal to 1, and Mundry and Gierer found that they did observe a maximum value for A4 when k t was 1 (the fraction of survivors is 37% when kt is equal to l), and also that reasonably good agreement was found between experimental values for M / M,,,, at different kt‘s and the theoretical values derived from the above equation.

25 26 26 27 28 29 31 31 33 42 43 44 45 46 47 55 58 I. INTRODUCTION One of the outstanding problems of biology is the nature of the relationship between gene and gene product. Viruses offer a useful material for attacking this problem because virus particles consist of a small number of genes and one to several gene products. The smalI ribonucleic acid-containing viruses are particularly useful for this purpose because many of them contain only enough nucleic acid to comprise a small number of genes and only a single species of protein as a gene product.

Chemical Mutagenesis In contrast to the absence of conclusive evidence for mutagenicity of in vivo treatments of the virus-host system or of irradiation of virus preparations in uitro, little doubt exists concerning the mutation-inducing power of at least one chemical reagent, nitrous acid. The chief reason for the Iack of uncertainty lies in an exceptionally high frequency mutation induction with this reagent. a. Nitrous Acid. i. The killing and mutagenic effect of nitrous acid. The efficacy of nitrous acid as a mutagen for TMV was first demonstrated by Mundry and Gierer (1958) (see also Gierer and Mundry, 1958).

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