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)

Constitutive mechanistic explanations are said to refer to mechanisms that constitute the phenomenon-to-be-explained. The most prominent approach of how to understand this constitution relation is Carl Craver’s mutual manipulability approach to constitutive relevance. Recently, the mutual manipulability approach has come under attack (Leuridan 2012; Baumgartner and Gebharter 2015; Romero 2015; Harinen 2014; Casini and Baumgartner 2016). Roughly, it is argued that this approach is inconsistent because it is spelled out in terms of interventionism (which is an approach to causation), whereas (...) constitutive relevance is said to be a non-causal relation. In this paper, I will discuss a strategy of how to resolve this inconsistency, so-called fat-handedness approaches (Baumgartner and Gebharter 2015; Casini and Baumgartner 2016; Romero 2015). I will argue that these approaches are problematic. I will present a novel suggestion of how to consistently define constitutive relevance in terms of interventionism. My approach is based on a causal interpretation of mutual manipulability, where manipulability is interpreted as a causal relation between the mechanism’s components and temporal parts of the phenomenon. (shrink)

Causal Bayes nets (CBNs) can be used to model causal relationships up to whole mechanisms. Though modelling mechanisms with CBNs comes with many advantages, CBNs might fail to adequately represent some biological mechanisms because—as Kaiser (2016) pointed out—they have problems with capturing relevant spatial and structural information. In this paper we propose a hybrid approach for modelling mechanisms that combines CBNs and cellular automata. Our approach can incorporate spatial and structural information while, at the same time, it comes with all (...) the merits of a CBN representation of mechanisms. (shrink)

Chronic myeloid leukemia (CML) is a cancer of the hematopoietic system initiated by a single genetic mutation which results in the oncogenic fusion protein Bcr-Abl. Untreated, patients pass through different phases of the disease beginning with the rather asymptomatic chronic phase and ultimately culminating into blast crisis, an acute leukemia resembling phase with a very high mortality. Although many processes underlying the chronic phase are well understood, the exact mechanisms of disease progression to blast crisis are not yet revealed. In (...) this paper we develop a mathematical model of CML based on causal Bayesian networks in order to study possible disease progression mechanisms. Our results indicate that an increase of Bcr-Abl levels alone is not sufficient to explain the phenotype of blast crisis and that secondary changes such as additional mutations are necessary to explain disease progression and the poor therapy response of patients in blast crisis. (shrink)