Utilization of Labelled ‘Myleran’ for the Determination of the Size of DNA Molecules in Cells

Abstract

THE mutagenic action of the electrophilic alkylating agents has been attributed to many different causes. For Alexander and Stacey¹, the alkylation of the DNA phosphates could be sufficient to induce mutations; but these could also be the consequence of the hydrolysis of the very unstable triester phosphate formed, with rupture of the macromolecule followed by large deletions. Lawley and Brookes² have postulated that the 7-alkylation of guanine makes this base couple with thymine instead of cytosine and so is responsible for transitions. But the alkylation of the guanine and adenine residues can also be followed by the loss of the alkylated base³; this depurination might act in two ways: the hole left gives the opportunity for transitions, transversions or nucleotide deletions when, the DNA replicates, or the DNA sugar-phosphate ‘backbone’ can break with loss of a part of the chain. All these chemical mechanisms damage only one helix of the DNA molecule exposed to the mono- or bi-functional alkylating drug and the mutation ought to appear only in one half of the genomes of the following generations.