Showing papers by "Daniel M. Brown published in 1969"
TL;DR: In this article, it was shown that in aqueous solution pyrimidines and purines form vertical stacks with no evidence of in-plane hydrogen-bonding between pairs of bases.
Abstract: RECENT spectroscopic work has shown that in aqueous solution pyrimidines and purines form vertical stacks with no evidence of in-plane hydrogen-bonding between pairs of bases1,2. The conformations of polynucleotides in aqueous solution are probably largely determined by the interactions responsible for the vertical stacking of mono-meric species3. In non-aqueous solution, vertical stacking is much less important1,4, and studies of mixtures of the nucleic acid bases indicate specific hydrogen-bonding between those pairs of bases that are complementary in DNA4–10. In solvents which are not hydrogen-bond donors, regardless of polarity, the association constant for the guanine–cytosine pair is several times greater than that for the adenine–thymine (uracil) pair, but in both cases the mixed complex is preferred to a mixture of self-dimers; mixtures of non-complementary bases show no association, although mixed hydrogen-bonded pairs can in principle be drawn.
8 citations
TL;DR: The view has become established with considerable certainty that the points on the map represent in many cases single base-pairs and the regions more or less extensive parts of the bacteriophage DNA.
Abstract: Since the realisation that the genetic material in living organisms is deoxyribonucleic acid (DNA) [or ribonucleic acid (RNA) in RNA-contaming viruses], the way has, in principle, been open for an attack on the question of the chemical basis of biological mutation. In this paper I wish to draw some conclusions respecting one mutagen, but, more importantly, try to demonstrate the nature of the problems involved and the kind of questions that must be asked. As background, it is necessary first, to recall that the understanding of the genetics of micro-organisms and the molecular basis thereof, has expanded enormously in recent years; this is particularly so of bacterial virus (bacteriophage) genetics'. The T even phages contain DNA in the form of a linear double-helical molecule containing of the order of 200 000 base-pairs. Using purely genetic methods Benzer2' was able to make a fine structure map of the rh-gene in T4, to which much more detail has since been added4. It is a map consisting of many points or regions in linear array and for each point or region, there is a T4r mutant (defective in the function that the r region controls). Map distances are, in fact recombinational frequencies derived from crossing mutants pair-wise in a suitable host bacterium. Although the scale may be badly distorted at short map distances5, nevertheless the view has become established with considerable certainty that the points on the map represent in many cases single base-pairs and the regions more or less extensive parts of the bacteriophage DNA. Of the several hundred ru mutants (and the many thousand in other genetic material) that have been studied some arose spontaneously and others were chemically induced. From the standpoint of chemical mutagenesis bacteriophages are valuable experimental material since they can be treated with the reagent in the test-tube and then, in the absence of excess reagent, replicated in the host bacterium allowing mutations, if any, to be expressed. As a result of genetic and chemical considerations, several types of mutational change have been recognised. These are listed in Table 1 and have
2 citations