Genetics was established on a strict particulate conception of heredity. Genetic linkage, the deviation from independent segregation of Mendelian factors, was conceived as a function of the material allocation of the factors to the chromosomes, rather than to the multiple effects (pleiotropy) of discrete factors. Although linkage maps were abstractions they provided strong support for the chromosomal theory of inheritance. Direct Cytogenetic evidence was scarce until X-ray induced major chromosomal rearrangements allowed direct correlation of genetic and cytological rearrangements. Only with (...) the discovery of the polytenic giant chromosomes in Drosophila larvae in the 1930s were the virtual maps backed up by physical maps of the genetic loci. Genetic linkage became a pivotal experimental tool for the examination of the integration of genetic functions in development and in evolution. Genetic mapping has remained a hallmark of genetic analysis. The location of genes in DNA is a modern extension of the notion of genetic linkage. (shrink)

William Bateson (1861-1926) has long occupied a controversial role in the history of biology at the turn of the twentieth century. For the most part, Bateson has been situated as the British translator of Mendel or as the outspoken antagonist of W. F. R. Weldon and Karl Pearson's biometrics program. Less has been made of Bateson's transition from embryologist to advocate for discontinuous variation, and the precise role of British and American influences in that transition, in the years leading up (...) to the publication of his massive Materials for the Study of Variation (1894). In this paper, I first attempt to trace Bateson's development in his early career before turning to search for the development of the moniker "anti-Darwinist" that has been attached to Bateson in well-known histories of the neo-Darwinian Synthesis. (shrink)

In addition to his experiments on selection in pure lines, Wilhelm Johannsen performed less well-known hybridisation experiments with beans. This article describes these experiments and discusses Johannsen’s motivations and interpretations, in the context of developments in early genetics. I will show that Johannsen first presented the hybridisation experiments as an additional control for his selection experiments. The latter were dedicated to investigating heredity with respect to debates concerning the significance of natural selection of continuous variation for evolution. In the course (...) of the establishment of a Mendelian research program after 1900, the study of heredity gained increasing independence from questions of evolution, and focused more on the modes and mechanisms of heredity. Further to their role as control experiments, Johannsen also saw his hybridisation experiments as contributing to the Mendelian program, by extending the scope of the principles of Mendelian inheritance to quantitative characters. Towards the end of the first decade of genetics, Johannsen revisited his experiments to illustrate the many–many relationship between genes and characters, at a time when that relationship appeared increasingly complex, and the unit-character concept, accordingly, became inadequate. For the philosophy of science, the example shows that experiments can have multiple roles in a research programme, and can be interpreted in the light of questions other than those that motivated the experiments in the first place. (shrink)

The concept of dominance poses several dilemmas. First, while entrenched in genetics education, the metaphor of dominance promotes several misconceptions and misleading cultural perspectives. Second, the metaphors of power, prevalence and competition extend into science, shaping assumptions and default concepts. Third, because genetic causality is complex, the simplified concepts of dominance found in practice are highly contingent or inconsistent. The conceptual problems are illustrated in the history of studies on the evolution of dominance. Conceptual clarity may be fostered, I claim, (...) by viewing diploid organisms as diphenic and by framing genetic causality modestly through individual alleles and their corresponding haplophenotypes. (shrink)