Marcel Weber

I defend the view that single experiments can provide a sufficient reason for preferring one among a group of hypotheses against the widely held belief that “crucial experiments” are impossible. My argument is based on the examination of a historical case from molecular biology, namely the Meselson-Stahl experiment. “The most beautiful experiment in biology”, as it is known, provided the first experimental evidence for the operation of a semi-conservative mechanism of DNA replication, as predicted by Watson and Crick in 1953. I use a mechanistic account of explanation to show that this case is best construed as an inference to the best explanation (IBE). Furthermore, I show how such an account can deal with Duhem's well-known arguments against crucial experiments as well as Van Fraassen's “bad lot” argument against IBE.

I examine some philosophical arguments as well as current empirical research in molecular neurobiology in order to throw some new light on the question of whether neurological processes are deterministic or indeterministic. I begin by showing that the idea of an autonomous biological indeterminism violates the principle of the supervenience of biological properties on physical properties. If supervenience is accepted, quantum mechanics is the only hope for the neuro-indeterminist. But this would require that indeterministic quantum-mechanical effects play a role in the functioning of the nervous system. I examine several candidates of molecular processes where this could, in theory, be the case. It turns out that there is good news from recent work on ion channels. Unfortunately (for the indeterminist), this good news is neutralised at once by bad news.

I present a reconstruction of F.H.C. Crick's two 1957 hypotheses "Sequence Hypothesis" and "Central Dogma" in terms of a contemporary philosophical theory of causation. Analyzing in particular the experimental evidence that Crick cited, I argue that these hypotheses can be understood as claims about the actual difference-making cause in protein synthesis. As these hypotheses are only true if restricted to certain nucleic acids in certain organisms, I then examine the concept of causal specificity and its potential to counter claims about causal parity of DNA and other cellular components. I first show that causal specificity is a special kind of invariance under interventions, namely invariance of generalizations that range over finite sets of discrete variables. Then, I show that this notion allows the articulation of a middle ground in the debate over causal parity.