I examine to what extent accounts of mechanisms based on formal interventionist theories of causality can adequately represent biological mechanisms with complex dynamics. Using a differential equation model for a circadian clock mechanism as an example, I first show that there exists an iterative solution that can be interpreted as a structural causal model. Thus, in principle, it is possible to integrate causal difference-making information with dynamical information. However, the differential equation model itself lacks the right modularity properties for a (...) full integration. A formal mechanistic model will therefore have to leave out either noncausal or causal explanatory relations. (shrink)

Mechanisms are often characterized as causal structures and the interventionist account of causation is then used to characterize what it is to be a causal structure. The associated modularity constraint on causal structures has evoked criticism against using the theory as an account of mechanisms, since many mechanisms seem to violate modularity. This paper answers to this criticism by making a distinction between a causal system and a causal structure. It makes sense to ask what the modularity properties of a (...) given causal structure are, but not whether a causal system is modular tout court. The counter-examples to the interventionist account are systems in which a particular structure is modular in variables, but not in parameters. A failure of parameter-modularity does not by itself threaten the interventionist interpretation of the structure and the possibility of causally explaining with that structure, but it does mean that knowledge of the structure is not sufficient to constitutively explain system-level properties of the embedding system. (shrink)

Manipulablity theories of causation, according to which causes are to be regarded as handles or devices for manipulating effects, have considerable intuitive appeal and are popular among social scientists and statisticians. This article surveys several prominent versions of such theories advocated by philosophers, and the many difficulties they face. Philosophical statements of the manipulationist approach are generally reductionist in aspiration and assign a central role to human action. These contrast with recent discussions employing a broadly manipulationist framework for understanding causation, (...) such as those due to the computer scientist Judea Pearl and others, which are non-reductionist and rely instead on the notion of an intervention. This is simply an appropriately exogenous causal process; it has no essential connection with human action. This interventionist framework manages to avoid at least some of these difficulties faced by traditional philosophical versions of the manipulability theory and helps to clarify the content of causal claims. (shrink)

In many biological experiments, due to gene-redundancy or distributed backup mechanisms, there are no visible effects on the functionality of the organism when a gene is knocked out or down. In such cases there is apparently no counterfactual dependence between the gene and the phenotype in question, although intuitively the gene is causally relevant. Due to relativity of causal relations to causal models, we suggest that such cases can be handled by changing the resolution of the causal model that represents (...) the system. By decreasing the resolution of our causal model, counterfactual dependencies can be established at a higher level of abstraction. By increasing the resolution, stepwise causal dependencies of the right kind can serve as a sufficient condition for causal relevance. Finally, we discuss how introducing a temporal dimension in causal models can account for causation in cases of non-modular systems dynamics. (shrink)