Presume It Not: True Causes in the Search for the Basis of Heredity

Kyle Stanford has recently given substance to the problem of unconceived alternatives, which challenges the reliability of inference to the best explanation (IBE) in remote domains of nature. Conjoined with the view that IBE is the central inferential tool at our disposal in investigating these domains, the problem of unconceived alternatives leads to scientific anti-realism. We argue that, at least within the biological community, scientists are now and have long been aware of the dangers of IBE. We re-analyze the nineteenth-century study of inheritance and development (Stanford’s case study) and extend it into the twentieth century, focusing in particular on both classical Mendelian genetics and the studies by Avery et al. on the chemical nature of the hereditary substance. Our extended case studies show the preference of the biological community for a different methodological standard: the vera causa ideal, which requires that purported causes be shown on non-explanatory grounds to exist and be competent to produce their effects. On this basis, we defend a prospective realism about the biological sciences

Presume It Not: True Causes in the Search for the Basis of Heredity

Kyle Stanford has recently given substance to the problem of unconceived alternatives, which challenges the reliability of inference to the best explanation (IBE) in remote domains of nature. Conjoined with the view that IBE is the central inferential tool at our disposal in investigating these domains, the problem of unconceived alternatives leads to scientific anti-realism. We argue that, at least within the biological community, scientists are now and have long been aware of the dangers of IBE. We re-analyze the nineteenth-century study of inheritance and development (Stanford’s case study) and extend it into the twentieth century, focusing in particular on both classical Mendelian genetics and the studies by Avery et al. on the chemical nature of the hereditary substance. Our extended case studies show the preference of the biological community for a different methodological standard: the vera causa ideal, which requires that purported causes be shown on non-explanatory grounds to exist and be competent to produce their effects. On this basis, we defend a prospective realism about the biological sciences

The Prodigal Genetics Returns: Integrating Gene Regulatory Network Theory Into Evolutionary Theory

The aim of this dissertation is to show how gene regulatory network (GRN) theory can be integrated into evolutionary theory. GRN theory, which lies at the core of evolutionary-developmental biology (evo-devo), concerns the role of gene regulation in driving developmental processes, covering both how these networks function and how they evolve. Evolutionary and developmental biology, however, have long had an uneasy relationship. Developmental biology played little role in the establishment of a genetic theory evolution during the modern synthesis of the early to mid 20th century. As a result, the body of evolutionary theory that descends from the synthesis period largely lacks obvious loci for integrating the information provided by GRN theory. Indeed, the relationship between the two has commonly been perceived, by both scientists and philosophers, as one of conflict. By combining historical and philosophical analysis, I consider four sources of tension between evo-devo and synthesis-derived evolutionary theorizing in order to show how those tensions can be resolved. I present a picture of the conceptual foundations of evo-devo that reveals the potential for integrating it with existing evolutionary theorizing. In chapter two, I argue that a major historical source of tension between evolutionary and developmental biology was the debates, in the first half of the 20th century, about the possibility of explaining development in terms of gene action. I show that the successes of GRN theory put these worries to bed. In chapter three, I argue that, rather than conceive of evo-devo as typological, we should see it as resting on Cuvieran functionalism. I argue that Cuvi-eran functionalism complements the Darwinian functionalism of the modern synthesis. In chapter four, I present a picture of the fine structure of the concept ‘homology’. This picture shows how accounts of homology that have traditionally been taken to conflict are in fact compatible and complementary. In chapter five, I analyze the nature of structure/function disputes in terms of types of answers to contrastive why-questions. On the basis of this analysis, I show how the structure of evolutionary theory requires both structuralist and functionalist approaches

Kon-Tiki Experiments

We identify a species of experiment—Kon-Tiki experiments—used to demonstrate the competence of a cause to produce a certain effect, and we examine their role in the historical sciences. We argue Kon-Tiki experiments are used to test middle-range theory, to test assumptions within historical narratives, and to open new avenues of inquiry. We show how the results of Kon-Tiki experiments are involved in projective (rather than consequentialist) inferences,and we argue (against Kyle Stanford) that reliance on projective inferences does not provide historical scientists with any special protection against the problem of unconceived alternatives

Kon-Tiki Experiments

We identify a species of experiment—Kon-Tiki experiments—used to demonstrate the competence of a cause to produce a certain effect, and we examine their role in the historical sciences. We argue Kon-Tiki experiments are used to test middle-range theory, to test assumptions within historical narratives, and to open new avenues of inquiry. We show how the results of Kon-Tiki experiments are involved in projective (rather than consequentialist) inferences,and we argue (against Kyle Stanford) that reliance on projective inferences does not provide historical scientists with any special protection against the problem of unconceived alternatives

Deep sequencing uncovers numerous small RNAs on all four replicons of the plant pathogen Agrobacterium tumefaciens

Agrobacterium species are capable of interkingdom gene transfer between bacteria and plants. The genome of Agrobacterium tumefaciens consists of a circular and a linear chromosome, the At-plasmid and the Ti-plasmid, which harbors bacterial virulence genes required for tumor formation in plants. Little is known about promoter sequences and the small RNA (sRNA) repertoire of this and other α-proteobacteria. We used a differential RNA sequencing (dRNA-seq) approach to map transcriptional start sites of 388 annotated genes and operons. In addition, a total number of 228 sRNAs was revealed from all four Agrobacterium replicons. Twenty-two of these were confirmed by independent RNA gel blot analysis and several sRNAs were differentially expressed in response to growth media, growth phase, temperature or pH. One sRNA from the Ti-plasmid was massively induced under virulence conditions. The presence of 76 cis-antisense sRNAs, two of them on the reverse strand of virulence genes, suggests considerable antisense transcription in Agrobacterium. The information gained from this study provides a valuable reservoir for an in-depth understanding of sRNA-mediated regulation of the complex physiology and infection process of Agrobacterium