It has been claimed that the intentional stance is necessary to individuate behavioral traits. This thesis, while clearly false, points to two interesting sets of problems concerning biological explanations of behavior: The first is a general in the philosophy of science: the theory-ladenness of observation. The second problem concerns the principles of trait individuation, which is a general problem in philosophy of biology. After discussing some alternatives, I show that one way of individuating the behavioral traits of an organism is (...) by a special use of the concept of biological function, as understood in an enriched causal role (not selected effect) sense. On this view, a behavioral trait is essentially a special kind of regularity, namely a regularity that is produced by some regulatory mechanism. Regulatory mechanisms always require goal states, which can only be provided by functional considerations. As an example from actual (as opposed to folk) science, I examine the case of social behavior in nematodes. I show that the attempt to explain this phenomenon actually transformed it. This supports the view that scientific explanation does not explain an explanandum phenomenon that is given prior to the explanation; rather, the explanandum is changed by the explanation. This means that there could be a plurality of stances that have some heuristic value initially, but which will be abandoned in favor of a functional characterization eventually. (shrink)

Watson and Crick’s discovery of the structure of DNA led to developments that transformed many biological sciences. But what were the relevant developments and how did they transform biology? Much of the philosophical discussion concerning this question can be organized around two opposing views: theoretical reductionism and layer-cake antireductionism. Theoretical reductionist and their anti-reductionist foes hold two assumptions in common. First, both hold that biological knowledge is structured like a layer cake, with some biological sciences, such as molecular biology cast (...) at lower levels of organization, and others, such as classical genetics, cast at higher levels. Second, both assume that scientific knowledge is structured by theory and that the productivity of scientific research depends on whether the underlying theory identifies the fundamentals upon which the phenomena to be explained and investigated depend. In the first part of this paper, I challenge these assumptions. In the second part, I show how recasting the basic theory of classical genetics made it possible to retool the methodologies of genetics. It was the investigative power of these retooled methodologies, and not the explanatory power of a gene-based theory, that transformed biology. (shrink)

The generalizations found in biology, psychology, sociology, and other high-level sciences are typically physically contingent. You might conclude that they play only a limited role in scientific investigation, on the grounds that physically contingent generalizations offer no or only feeble counterfactual support. But the link between contingency and counterfactual support is more complex than is commonly supposed. A certain class of physically contingent generalizations, comprising many, perhaps the vast majority, of those in the high-level sciences, provides strong counterfactual support of (...) just the sort that appears to be scientifically important. This paper explains why. (shrink)

I examine the adequacy of the causal graph-structural equations approach to causation for modeling biological mechanisms. I focus in particular on mechanisms with complex dynamics such as the PER biological clock mechanism in Drosophila. I show that a quantitative model of this mechanism that uses coupled differential equations – the well-known Goldbeter model – cannot be adequately represented in the standard causal graph framework, even though this framework does permit causal cycles. The reason is that the model contains dynamical information (...) about the mechanism that concerns causal properties but that does not correspond to variables that could be subject to independent interventions. Thus, a representation of the mechanisms as a causal structural model necessarily suppresses causally relevant information. (shrink)

Intertheoretic relations are an important topic in the philosophy of science. However, since their classical discussion by Ernest Nagel, such relations have mostly been restricted to relations between pairs of theories in the natural sciences. In this paper, we present a model of a new type of intertheoretic relation, called 'Montague Reduction', which is assumed in Montague's framework for the analysis and interpretation of natural language syntax. To motivate the adoption of our new model, we show that this model extends (...) the scope of application of the Nagelian (or related) models, and that it shares the epistemological advantages of the Nagelian model. The latter is achieved in a Bayesian framework. (shrink)

The paper describes the change from molecular genetics to postgenomic biology. It focuses on phenomena in the regulation of gene expression that provide a break with the central dogma, according to which sequence specificity for a gene product must be template derived. In its place we find what is called here ‘constitutive molecular epigenesis’. Its three classes of phenomena, which I call sequence ‘activation’, ‘selection’ and ‘creation’, are exemplified by processes such as transcriptional activation, alternative cis- and trans-splicing, and RNA (...) editing. These phenomena support the following main theses of the paper: 1. Other molecular resources share the causal role of ‘genes’: the ‘causal specificity’ for the linear sequence of any gene product is distributed between the coding sequence, cis-acting sequences, trans-acting factors, environmental signals, and the contingent history of the cell (the cellular code) (thesis of distributed causal specificity). 2. These multiple and overlapping processing and targeting mechanisms amplify the repertoire of RNA and protein products specified through the eukaryotic genome, expanding the possibilities specified by the literal code of DNA (thesis of genetic underdeterminism). 3. These mechanisms of gene expression change the focus of postgenomic research from single molecules and their molecular, biochemical and intrinsic function to their cellular, constituent, component or contextual function due to their recruitment and organization in complex cellular networks. In other words, all agents involved in the regulation of gene expression, including DNA, must interact with other agents to achieve full specificity, which is imposed by regulated recruitment and combinatorial control (theses of regulated recruitment and of system analysis). I conclude from these three main theses that the complexity of higher organisms lies not in its number of genes but in the flexibility, versatility and reactivity of its whole genome. (shrink)

This paper discusses three shortcomings of the current state of the debate regarding historical evidence against scientific realism. Attending to these issues will direct the debate away from over-generalising wholesale arguments.